Anatomy and Physiology: It's a Long Way Down

It's a Long Way Down

The mixture of masticated (chewed) food and saliva we swallow is called a bolus (sort of a big spit ball). The role of the pharynx, and especially the epiglottis, is discussed in The Respitory System. Quite an adventure will ensue, but the first leg of the journey is rather uneventful. The esophagus is less than a foot long (some 25 cm). Not being in constant use as with the trachea, it lacks the trachea's cartilaginous rings, opening mainly when we swallow. The esophagus is mainly a tube, somewhat lengthened to allow room for the thoracic organs; it doesn't even have a strong sphincter muscle at each end.

The muscular entrance, called the upper esophageal sphincter, is called such merely because it mimics the effect of a sphincter muscle. The exit, or the lower esophageal sphincter, is also called the cardiac sphincter, given its proximity to the heart. That name, however, sometimes causes some confusion, so it is increasingly known as the gastroesophageal sphincter. By putting the prefix gastro- before the esophagus, this helps to emphasize that the primary function of this “sphincter” is to prevent backflow, similar to, though less efficient than, the valves in the heart, in veins, and in lymphatic capillaries. When that backflow does happen, the poorly protected lining of the esophagus is digested by gastric juices, causing the sensation known as heartburn (there is no actual connection to the heart, except for the pain being felt behind the heart).

Protein Buster

Whenever people think about digestion, the first organ that comes to mind is the stomach. In fact, the stomach does very little digestion at all (liquids reside there for only about 1¹/₂ to 2¹/₂ hours, and solids anywhere from 3 to 4 hours). When asked to point to their stomachs, most people would probably point to the area of the umbilicus (“belly button”), and the idea of touching the bottom of the ribcage on the left side probably wouldn't occur to them. In many ways, the stomach is a surprising organ.

The expression “a full stomach” makes a lot of sense when you consider the many large folds in the lining of the gastric mucosa, known as rugae. These rugae (singular, ruga) allow the lumen of the stomach to expand after eating a large meal; you might be surprised to learn that the average adult's stomach can hold anywhere from 1 to 1¹/₂ liters of food! Is it any wonder that some people's clothes feel tighter after a big meal?

The contents of the stomach—a mixture of food, saliva, and gastric juices—are called chyme. It may surprise you to know that your stomach gets started before you even take your first bite! This first phase of gastric activity is called the cephalic phase (cephalic = head). In this phase the gastric secretions actually start as a result of seeing, smelling, tasting, or even thinking about food!

The second phase, aptly named the gastric phase, doesn't start until the food actually enters the stomach. At this stage, the change in pH—brought about by the cephalic phase—the presence of your chewed-up meal (especially the presence of protein, the stomach's forte), and the stretching of the stomach lining by that food, get the gastric phase into full gear. Gastrin, a hormone produced by the G-cells at the very bottom of the gastric pit, will increase gastric secretion—the irony is that, as a hormone, it must make a full circuit through the blood to get to the cells that are right next door! Stretch receptors also send nervous signals that ultimately lead to greater gastric juice.

The last phase, which starts up to four hours after the start of the gastric phase, is quite sensibly named the intestinal phase, is the one in which, as you can imagine, the chyme is sent on its merry way into the first part of the small intestine, the duodenum, through the pyloric sphincter (in this case, a real sphincter). The lion's share of the digestion happens in the small intestine, so it is important that the digestion happens efficiently. If too much food enters the small intestine at once, the enzymes will not be able to digest it all effectively.

This is regulated by something called the enterogastric reflex, in which a slowing of gastric contractions follows the “squirting” of chyme into the duodenum. This prevents too much chyme from entering the duodenum at once, and also enables the duodenum to prepare, through the production of extra buffers, to counteract the low pH of the gastric chyme. If this regulation doesn't function properly, a duodenal ulcer is the result!

Okay, you get the idea that the stomach releases digestive enzymes to digest proteins, but aren't there proteins on the outside of every cell, including those that line the stomach? So how does the stomach keep from digesting itself after pumping out so much stomach acid and enzymes? For one thing, it doesn't always! Sometimes the stomach starts to digest its own lining, basically turning itself into a cannibal! That, in a nutshell, is the basis of an ulcer—I know some people get hungry from time to time, but really! Still, most people never develop ulcers, so how does the stomach keep from eating itself?

For one thing, the gastric mucosa (which lines the lumen) makes good on its name and churns out large quantities of mucus. Since mucus is made of water, protein, and polysaccharides, the water helps to dilute the acid, thus raising (buffering) the pH of the gastric juice closest to the mucosa; the enzyme pepsin gets to work on the mucous proteins, rather than the mucosal proteins! That is all well and good, but what about when the HCl and the pepsin are first released? What protects the cells then?

In a tricky maneuver, the stomach takes advantage of the shape of the gastric mucosa, and a little chemical trickery, to get away with it (see Figure 14.3)! The gastric mucosa is filled with pits called gastric pits. At the base of these pits are chief cells, which release pepsinogen, an inactive form of the enzyme pepsin. Being inactive, the protein poses no problem for the mucosa. At the neck of these gastric pits are parietal cells, which release HCl acid. That alone would be a problem, but for the cell's clever habit of releasing H+ ions and Cl ions separately, thus protecting itself from the HCl acid! Sure, fine, but how does the pepsinogen turn into pepsin? By mixing with the HCl acid! Those two don't mix until they meet in the neck of the gastric pit, and the enzyme doesn't become active right away, thus buying enough time to wait for the chemicals to reach the lumen! This is just one more example of how true understanding of the anatomy of the body (in this case, of the gastric pits) is only understood when one also looks at the physiology!

The greatest risk when the stomach starts digesting itself is that such an ulcer can actually digest so deep a hole in the stomach wall that an opening is made into the abdominal cavity; this is called a perforated ulcer. Luckily, the body has an ace up its sleeve in a somewhat disgusting sheet of connective tissue called the greater omentum (see Figure 14.4). This sheet literally hangs down in front of the small intestine, acting in part as a place for depositing excess fat, but more importantly, the greater omentum can adhere to any perforations in the stomach wall, thus preventing the contents from emptying into the abdominal cavity. There is also a lesser omentum, but it just connects the liver to the stomach.