Diarrhoea transit-time - quick question

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Phloston

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From GT:

"The inability to break down the disaccharide lactose means that it is not absorbed. This dumps a high osmolar load in the colon, leading to decreased transit time (decreased water absorption), leading to diarrhea."

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Notice it says decreased transit time. Maybe I have yet to properly conceptualize the mechanism regarding osmotic diarrhoea, but wouldn't the transit time be the same in this case? It's not that feces are moving more quickly through the lumen; it's just that water is merely pulled into it. Therefore, wouldn't deranged motility be the only DOMES type to have decreased transit-time?

Could anyone please comment?

Cheers,

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I thought increased distention (e.g. water volume) leads to increased motility?
 
I thought increased distention (e.g. water volume) leads to increased motility?

Yes.

Just think about giving someone a big healthy dose of lactulose for their hepatic encephalopathy..a good example of drug induced osmotic diarrhea. If you have ever witnessed a patient take lactulose, they have to go in a hurry! The above reason is why this occurs...or at least it's what my impression has been. You distend the bowel which stimulates peristalsis, in turn decreasing transit time.
 
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Yes.

Just think about giving someone a big healthy dose of lactulose for their hepatic encephalopathy..a good example of drug induced osmotic diarrhea. If you have ever witnessed a patient take lactulose, they have to go in a hurry! The above reason is why this occurs...or at least it's what my impression has been. You distend the bowel which stimulates peristalsis, in turn decreasing transit time.

Could you please be very specific? I need a solid mechanism.
 
Man, I can't really see step I demanding such specific info. Or if they did you could probably reason it out.

Basic, high yield mechanism: bowel distension from increased osmotic load increases motility/peristalsis

Complicated sciency mechanism: I don't know. And I don't want to look it up because it will likely never be important in the clinical setting for me. Plus I'm not sure if it's really known for sure.

Good luck on your quest for knowledge :D
 
Man, I can't really see step I demanding such specific info. Or if they did you could probably reason it out.

Basic, high yield mechanism: bowel distension from increased osmotic load increases motility/peristalsis

Complicated sciency mechanism: I don't know. And I don't want to look it up because it will likely never be important in the clinical setting for me. Plus I'm not sure if it's really known for sure.

Good luck on your quest for knowledge :D

I appreciate the help. I would want to know why distension would increase peristalsis as opposed to just memorizing it.

If I had to reason through it, I would guess that distension would increase afferent baroreceptor firing, leading to increased PSNS efferent signaling via M3.

If that's even the case, then I'd further ask whether this is also the basis for mass movements of the transverse colon following the consumption of large meals..
 
It is definitely distention that causes the increase in bowel movement. I believe this is the basis for the urge to poop after a person eats. I forgot what the reflex is called though (maybe it was the ilocecal reflex). its somewhere in BRS physiology. I think its just the myenteric plexus that is involved in the increase in the increase in movement rather than the reflex via the parasympathetics.
 
It is definitely distention that causes the increase in bowel movement. I believe this is the basis for the urge to poop after a person eats. I forgot what the reflex is called though (maybe it was the ilocecal reflex). its somewhere in BRS physiology. I think its just the myenteric plexus that is involved in the increase in the increase in movement rather than the reflex via the parasympathetics.

That's the gastrocolic reflex, from stomach distention
 
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