|MadSci Network: Medicine|
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
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