MadSci Network: Medicine
Query:

Re: Why do you vomit bile when it's produced 'downstream' of the stomach ?

Date: Sat Nov 3 20:17:22 2001
Posted By: Joshua Chai, Medical student, Medical Sciences, University of Cambridge
Area of science: Medicine
ID: 1004049261.Me
Message:

Hi Dave,
To answer your question, we first need a background understanding of the 
control of the gastrointestinal tract motility and the mechanism governing 
vomiting. 

When we ingest food, the bolus is masticated and mixed with salivary 
enzyme inside our mouths. After this, a voluntary action of swallowing 
takes place whereby the soft palate is raised, the epiglottis sealed 
against the entrance of the trachea, and the tongue is also raised and 
pushed against the palate so that to propel the bolus/chyme into the upper 
segment of the oesophagus. The oesophagus is composed of both striated and 
smooth muscle, and there is a gradual transition of voluntary action to 
involuntary peristalsis when the chyme travels down the oesophagus. 
Peristalsis is the combination of a number of local reflexes:- (adapted 
from Instant Physiology)

1.	Mucosal stimulation and/or distension of the gut lumen release 5-HT
2.	This produces circular muscle contraction above the stimulus via 
ascending cholinergic interneurons to excitatory motor neurons (containing 
acetylcholine and substance P).
3.	Below the stimulus, descending cholinergic interneurons activate 
inhibitory motor neurons (containing NO, VIP and ATP) and cause muscle 
relaxation.
4.	This propels the bolus of food forward.

Another important event that we must consider in order to attempt your 
question is gastric emptying. There are several factors which control 
gastric emptying and they can be split into two sections - signals from 
the stomach and signals from the duodenum. In general the signals from the 
stomach stimulate emptying are weak in comparison to control exerted by 
the duodenum. Particularly strong contractions occur in the stomach while 
mixing is going on, which serve to sweep the chyme down to the pylorus. 
This results in more liquid being forced through the pylorus than during 
retropulsion. These strong contractions occur in response to distension of 
the stomach i.e. the presence of food. Gastrin is secreted in the stomach 
in response to food and acid and this peptide also exerts a stimulatory 
effect on stomach emptying.
The duodenum primarily controls the rate of stomach emptying as efficient 
digestion and absorption is dependent on emptying chyme into the duodenum 
at an appropriate rate. When food enters the duodenum sensory receptors in 
the wall are stimulated which cause reflexes to feedback onto stomach 
activity and inhibit emptying. These receptors are stimulated by 
distension, and constituents of food such as lipids. If the stimulus is 
powerful enough for example something extremely irritating stomach 
emptying can be completely stopped. The reflexes can be extremely rapid, 
particularly those mediated by the enteric nervous system, and are 
particularly sensitive to irritants and acid of pH < 4.
Humoral factors primarily cholecystokinin or CCK are released by the 
presence of peptides , amino acids and importantly fats in the jejunum. 
CCK is particularly effective at decreasing gastric emptying by blocking 
the effect of gastrin on stomach motility.
The strong inhibitory stimuli from the intestine i.e. the enterogastric 
reflexes and the humoral factors act together to control the rate of 
gastric emptying so that efficient absorption and digestion can occur. 
These mechanisms are activated when there is either too much chyme in the 
duodenum, by distension and food products, or if the chyme is unprocessed 
i.e. it is too acid, has too much unbroken down fat or protein or is 
irritating.

As you can see, GI tract motility is coordinated by both gut hormones and 
the enteric nervous system, which is further regulated by vagal 
innervation (e.g. vago-vagal reflexes). These well-coordinated actions 
could normally prevent regurgitation of food/reverse peristalsis; however, 
there is also a special centre in our brainstem that can override all 
these control mechanisms and initiate the vomiting reflex. The vomiting 
centre can be directly stimulated by drugs (e.g. apomorphine); or by 
signals transmitted via nervous pathways from the stomach (after ingesting 
irritating substances or in stomach disease, such as peptic ulceration or 
pyloric stenosis), the intestine (e.g. in intestinal obstruction), or from 
the inner ear (as in motion sickness). The stimulated vomiting centre then 
sets off trains of nerve impulses to produce a stereotyped sequence of 
events, this includes powerful contraction of the abdominal muscle which 
raises intra-abdominal pressure to serve the propulsion of chyme upward; 
this is then accompanied by coordinated contraction and relaxation of the 
diaphragm so that stomach content can be expelled. 

Note that the pylorus is a thickened area of gastric muscle which is in a 
tonic state of contraction. It usually remains contracted although it can 
be modulated. This means that even in normal physiological state small 
volumes of liquid can usually pass through the pylorus into the duodenum. 
So when the vomiting centre is overwhelmingly stimulated, the reverse can 
also happen, i.e. intra-abdominal pressure can be raised to so high that 
duodenal content (may contain bile), or indeed content from the proximal 
ileum, can be forced to travel upward through the pylorus to enter the 
stomach against peristalsis. In cases like this, you may experience the 
presence of more watery content in your vomit in which bile may 
occasionally be found. Of course, you do need something pretty nasty to 
stimulate your stomach (and your vomit centre) to that extent!!

I hope this answered your question:-)

Joshua Chai
Medical Student
University of Cambridge, UK


Current Queue | Current Queue for Medicine | Medicine archives

Try the links in the MadSci Library for more information on Medicine.



MadSci Home | Information | Search | Random Knowledge Generator | MadSci Archives | Mad Library | MAD Labs | MAD FAQs | Ask a ? | Join Us! | Help Support MadSci


MadSci Network, webadmin@www.madsci.org
© 1995-2001. All rights reserved.