Each of the three agents acts only on cells having receptors for that agent. Because hormones travel through the general circulation, receptors are responsible for specificity. In the case of paracrines, the cells containing a specific receptor must also be located in near proximity to the site of release in order for the agent to reach them by diffusion. Target cells for neurocrines must be present in the synapse where the agent is released.

Serum gastrin levels are increased because the tumor secretes gastrin. Fat content in the stool is increased, because the large amounts of acid entering the duodenum inactivate pancreatic lipase and precipitate bile acids necessary for fat digestion and absorption. Parietal cell number is increased due to the trophic effect of gastrin. Antral gastrin release is decreased, because increased gastric acid secretion increases somatostatin release, which inhibits antral gastrin release. Histamine release increases because gastrin releases histamine, which then adds to the increased stimulation of acid secretion. Secretin increases gastrin release from gastrinomas even though it inhibits antral gastrin release.

These terms indicate whether or not a reflex leaves the GI tract via the extrinsic nervous system or whether it occurs entirely within the GI tract and the intrinsic enteric nervous system. Short reflexes can control certain activities such as some aspects of peristalsis without any influence from higher centers. Long reflexes, which are usually vago-vagal, meaning that both afferent and efferent neurons are part of the vagus nerve, allow signals from the GI tract to be processed and integrated within the brainstem to produce a coordinated response in the GI tract.

Each contraction in both tissues must be preceded and triggered by a slow wave. But every slow wave does not necessarily cause a contraction. The ability of a slow wave to cause a contraction depends on neural and hormonal activity in the tissue involved. Thus during a meal, there is increased vagal activity and hormone release, which may increase the amplitude of gastric slow waves or the frequency of spiking on intestinal slow waves, both of which increase the ability of a slow wave to initiate a contraction in its respective tissue. The actual frequency of slow waves, however, remains unchanged and that frequency is the same as the maximum possible rate of contraction if every slow wave were to stimulate a contraction.

The vagus nerve directly innervates the cells of the striated muscle while it innervates interneurons of the smooth muscle portion. This means that cervical vagotomy will prevent peristalsis in the striated portion but not in the smooth muscle portion. The fact that local nerves innervate the smooth muscle cells and communicate with each other allows peristalsis to take place in vitro following stimulation.

Because the esophagus is flaccid, its intraluminal pressure is negative reflecting that of the thorax. Sphincters prevent air from entering the upper esophagus and gastric juice (acid) from entering the lower esophagus. The importance of the lower esophageal sphincter (LES) is readily apparent in cases of gastric esophageal reflux disease in which intra-gastric pressures increase, LES pressure decreases or hiatal hernia, each of which increases the possibility for gastric acid to enter the esophagus.

A physiological action of CCK is the inhibition of gastric emptying. Thus you would expect a relaxation of the orad stomach, which would decrease intragastric pressure; a decrease in the frequency and force of contractions of the antrum and caudad stomach; an increase in the force or rate of contraction of the pylorus; and an increase in the segmenting activity of the duodenum.

The only one of the choices that is digested by pancreatic enzymes is starch. Thus pancreatic amylase digests starch into a hypertonic solution of maltose, maltotriose, and dextrins. This hypertonic solution would trigger a reflex from the duodenum to inhibit gastric emptying, so in the absence of sufficient pancreatic enzymes the isotonic starch would empty more rapidly than normal.

Gastric slow waves vary in amplitude and must reach threshold in order to stimulate a contraction. When threshold is reached, one or more spike potentials are triggered that result in muscle contractions. Thus, gastric slow waves are similar to action potentials. At all sites in the stomach, the frequency of slow waves is the same at approximately three cycles per minute. At any one site in the small bowel, the amplitude of the slow waves is constant, and contractions are initiated by a second electrical event that occurs only during the depolarization phase of the slow wave. Thus in the small bowel slow waves do not trigger contractions. At different sites the slow wave frequency in the small bowel varies, decreasing from approximately 12 cycles per minute in the duodenum to approximately 8 cycles per minute in the distal ileum.

Almost all significant digestion and absorption of nutrients take place in the small intestine. The major motility pattern of the small bowel in the presence of food is segmentation, which mixes the food with digestive enzymes and fluid and exposes the breakdown products to the absorptive surface of the intestine. Segmentation does not result in significant aboral propulsion, which optimizes the time needed for digestion and absorption. Additional brief peristaltic contractions move material distally over short segments of intestine.

The ileocecal reflex refers to a sphincteric mechanism at the ileocecal junction that regulates the movement of material through the junction. When the pressure in the ileum increases, the sphincter relaxes, allowing material to move into the colon. When the pressure in the proximal colon increases, the sphincter contracts, preventing reflux into the ileum. The tone of the sphincter is basically myogenic, but changes in tone in response to distention of the ileum and colon are mediated by local enteric nerves.

Most of the contractions of the ascending and transverse colon are segmental, and at adjacent sites are independent of each other. Thus, the material in the colon is slowly moved back and forth exposing it to the mucosa, where additional water and electrolytes are absorbed, reducing its volume. Of the 600 to 700 mL of water that enter the colon, only 100 to 150 mL normally appear in the feces. Occasionally segmental contractions are organized into a mass movement that propels luminal contents in an aboral direction making room for additional materials. Additional water is removed in the descending and sigmoid colon, and material becomes a semi-solid. The motility pattern of the distal colon is also segmentation but it is nonpropulsive and prevents material from entering the rectum until a subsequent mass movement occurs.

In contrast to other GI secretions, saliva is hypoosmotic at all rates of secretion and contains high amounts of potassium, which may even approach intracellular concentrations. Saliva is produced in volumes that far exceed those of the secretions of other organs on a per weight basis. The rate of secretion is controlled almost entirely by neural input without any hormonal stimulation such as that for gastric and pancreatic secretion. Finally both the parasympathetic and sympathetic systems stimulate salivary secretion.

As saliva moves through the duct, K ⁺ is secreted and Na ⁺ and Cl ^– are reabsorbed. Therefore the K ⁺ concentration will be higher and those of Na ⁺ and Cl ^– will be lower. Because <SPAN role=presentation tabIndex=0 id=MathJax-Element-1-Frame class=MathJax style="POSITION: relative" data-mathml='HCO3−’>HCO−3HCO3−
HCO 3 −
is secreted, its concentration will increase. The duct is relatively impermeable to water, and more Na ⁺ and Cl ^– are reabsorbed than K ⁺ and <SPAN role=presentation tabIndex=0 id=MathJax-Element-2-Frame class=MathJax style="POSITION: relative" data-mathml='HCO3−’>HCO−3HCO3−
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are secreted, so the saliva will be hypotonic at the duct opening.