The mouth, or oral cavity, is the usual point of entry for nutrients and is the site of the initial breakdown of nutrient substances into a form usable by the body. Food is pushed toward the side of the mouth by the tongue to facilitate chewing and grinding on the surfaces of the molar and premolar teeth. As the food is manipulated and broken down, it is moistened by saliva secreted by three major pairs of salivary glands: the parotid, submandibular, and sublingual glands (Figure 35-2). Saliva serves three major functions: (1) by its moistening action, saliva allows the tongue to convert a mouthful of food into a bolus, or semisolid mass, that can be swallowed easily; (2) it allows for taste perception by the papillae on the surface of the tongue, which are sensitive to chemical differences among dissolved food molecules; and (3) the digestive enzyme contained in saliva, salivary amylase (also called ptyalin), initiates carbohydrate digestion by breaking down polysaccharides (also called starch) into the simpler molecular structures of dextrin and maltose.^6,7 Important changes in oral structure and function that occur with aging are detailed in Geriatric Considerations: Changes in the Mouth.

GERIATRIC CONSIDERATIONS

Changes in the Mouth

Elderly people experience a decline in taste. This decline is due to both an increase in the sensation threshold for all four tastes and a decrease in the number of papillae. For example, children have more than 200 taste buds, whereas the elderly have fewer than 100. Of the four basic tastes, elderly people experience a particular decrease in salt and sugar tastes.

Older individuals also experience a decrease in the number of acinar cells in the salivary glands, leading to a reduction in salivary secretion. These changes can contribute to halitosis (bad breath).

Loss of teeth in the elderly is due to atrophy of gum and bone tissue as well as actual tooth deterioration. As tooth enamel is destroyed, dentin is exposed, allowing development of caries (cavities). Gingival epithelial loss may occur as a result of pathologic processes as well as normal aging.

The pharynx, or throat, is about 12 cm long and serves as the entryway for both the respiratory and the GI systems. The oropharynx, the portion of the pharynx posterior to the mouth, is separated from the nasopharynx, the portion of the pharynx posterior to the nose, by the soft palate. The laryngopharynx is the portion of the pharynx that opens into the larynx and the esophagus. During swallowing, the soft palate is pulled upward to close off the nasopharynx. The bolus of food being swallowed is propelled by reflex movements of muscles in the pharynx through the laryngopharynx and into the esophagus. Simultaneously, the opening to the larynx is closed by the epiglottis. This coordinated set of actions prevents food substances and liquids from inadvertently entering the respiratory system, a potentially life-threatening occurrence referred to as aspiration.

The esophagus is a muscular tube approximately 25 cm in length that initiates the progress of food through the gut after ingestion. Passage of food through the esophagus is greatly facilitated by mucus secreted by cells in the epithelial lining. Extremely rough or fibrous foods may potentially penetrate the mucous lining of the esophagus and cause damage. The stratified squamous epithelium lining the esophagus is constantly renewed by cells moving to the surface from below, thus providing a means of epithelial renewal. The esophagus propels nutrients to the stomach by means of strong muscular contractions. (Presbyesophagus, or abnormal esophageal motility occurring with advanced age, is described in detail in the Age-Related Changes section.) When the body is in an upright position, gravity assists in the downward movement of food to the stomach. However, the muscular contractions of the esophagus are extremely strong and are sufficient to transport nutrients to the stomach even in the absence of gravity, as persons living (and eating) in the weightless conditions of space have demonstrated.1,3

At the lower end of the esophagus, about 2 to 5 cm above its juncture with the stomach, the circular muscle of the esophagus functions as a sphincter; this region is referred to as the lower esophageal sphincter (LES). Although anatomically this sphincter is no different from the remainder of the esophagus, it remains tonically constricted, in contrast to the middle and upper portions of the esophagus, which are completely relaxed under normal conditions.² Thus the LES serves to prevent the highly acidic gastric contents from moving in a retrograde motion back into the esophagus. Under certain conditions the LES does not function properly, and reflux of gastric contents into the esophagus gastroesophageal reflux disease (GERD) may occur. The resulting subjective sensation of irritation and spasms of the distal portion of the esophagus is often referred to as heartburn or dyspepsia.

The stomach (Figure 35-3) is essentially an elastic food reservoir. Under normal circumstances, its capacity is 1000 to 1500 ml, although a capacity of as much as 6000 ml is possible.² The portion of the stomach immediately below the LES is called the cardia. The fundus is the part of the stomach that continues lateral to and above the cardia; the body of the stomach extends from the cardia to the antrum, which stretches from the angulus to the pylorus. The antrum differs markedly from the rest of the stomach in function and is distinguished by the absence of rugae, the folds present in the mucous membrane of the other areas of the stomach. The pylorus is a muscular sphincter between the stomach and duodenum that serves to control gastric emptying and limits the reflux of bile from the small intestine.

The stomach is lined with simple columnar epithelium containing millions of gastric glands that extend down to the mucosa. A typical gastric gland is shown in Figure 35-4. As shown in this illustration, gastric glands are lined by several types of specialized cells. Chief cells produce pepsinogen, the inactive form of the enzyme pepsin; parietal cells produce hydrochloric acid and also a substance called intrinsic factor that is needed for adequate intestinal absorption of vitamin B₁₂.⁸ Mucous cells produce an alkaline mucus that serves to shield the stomach wall and neutralize the acidity in the immediate area of the lining. A layer of mucus more than 1 mm thick continuously bathes the free surfaces of the gastric epithelial lining. In addition to these cells, gastrin cells are located in the antral epithelium and have surface microvilli that monitor intragastric pH. The role of these cells and the substances they secrete in the digestion of nutrients are described in detail in the Secretory Function section.

On microscopic examination, the lining of the small intestine contains millions of fingerlike projections called intestinal villi (Figure 35-5). Like the circular folds just described, these villi serve to increase the surface area of the intestine for digestion and absorption of nutrients. Each villus has its own microscopic projections called microvilli, which in turn are covered by a fuzzy coat (called the brush border because of its brushlike appearance when viewed with an electron microscope) containing many digestive enzymes. The combined effect of the circular folds, villi, and microvilli is to increase the surface area of the small intestine by about 600 times, thereby creating a remarkably efficient interface for nutrient digestion and absorption. Figure 35-6 shows a microscopic section of the small intestine.

The large intestine (Figure 35-7) is a muscular tube 1.5 m long and 6.5 cm in diameter that forms a frame around the small intestine. The portion of the large intestine from the cecum to the rectum is known as the colon. The ascending colon extends from the cecum straight up to the lower border of the liver; the transverse colon then extends across the abdomen, anterior to the small intestine. The descending colon turns downward on the left side of the abdomen, finally becoming the S-shaped sigmoid colon, which empties into the rectum. The rectum has its outlet at the anus, the opening for elimination of feces (see Figure 35-7).

The vermiform appendix, attached to the cecum, is a worm-shaped blind tube containing specialized lymphatic structures. It contains T and B lymphocytes, secretes immunoglobulin A (IgA), and contributes to gut-associated lymphoid function.9 Inflammation of the appendix, or appendicitis, is a life-threatening occurrence that can lead to peritonitis if not diagnosed and managed promptly.

The mucosa of the large intestine has no villi and does not produce digestive enzymes (Figure 35-8). The epithelial surface of the colon consists of absorptive cells that predominantly absorb water and electrolytes.¹⁰ Mucus-producing goblet cells line the glandular crypts present in the surface epithelium. Endocrine cells are also present, perhaps helping coordinate colon neurologic activity, but at present the function of hormones in the large intestine is poorly understood. The turnover time of cells in the colonic mucosa is 3 to 8 days, comparatively longer than that of cells in the small intestine.

The sympathetic fibers that innervate the GI tract have their origin in the spinal cord between T8 and L3. After exiting the cord, the preganglionic fibers enter the sympathetic chains and then pass through these chains to various ganglia adjacent to the GI tract, such as the celiac ganglion and the mesenteric ganglia. From these locations, postganglionic fibers radiate out to all parts of the gut. These sympathetic fibers supply essentially all parts of the GI tract (in contrast to the concentration of parasympathetic innervation at locations close to the entry and exit points of the gut).2 The sympathetic nerve endings in the GI tract secrete norepinephrine, which promotes the inhibitory effect of the sympathetic nervous system on the GI tract in the following ways: Norepinephrine acts directly on smooth muscle in the GI tract to inhibit activity; in addition, norepinephrine has an inhibitory effect on the neurons of the intrinsic nervous system of the GI tract. Strong stimulation of the sympathetic nervous system can effectively stop motility in the gut and therefore block the movement of nutrients through the GI tract. Gastrointestinal sympathetic activity can also initiate vomiting through a complex sequence of events mediated by various neurotransmitters.^13–15

Electrical activity is almost constantly present in the smooth muscle layers of the GI tract. Two basic types of electrical wave activity have been identified in the gut: slow waves and spikes (the latter named for the spiking appearance of these sudden increases in membrane potential).1,2 These two types of electrical wave patterns are shown in Figure 35-10. Slow-wave electrical activity represents an ongoing basic oscillation in membrane potential that occurs in the smooth muscle of the GI tract, especially in the muscle in the longitudinal layer. Normally, between 3 and 12 slow waves occur per minute, ranging from 40 to 50 millivolts (mV) in amplitude. Slow waves can be any degree of intensity and are not the “all-or-nothing” type of action potential seen in other smooth muscle fibers in the body. In contrast to these nearly continuous slow waves, spikes occur under certain circumstances. When the muscle layer in the GI tract is stimulated by being stretched or by the effects of acetylcholine or parasympathetic excitation, the intracellular resting membrane potential of the muscle fibers becomes relatively more positive. The entire potential level of the slow waves is raised—an effect called depolarization.¹ As shown in Figure 35-10, when depolarization rises above a certain level (around −40 mV), sudden increases in the membrane potential, or spikes, start to appear on the peaks of the slow waves. If the resting potential rises further, spikes appear more frequently. With very strong stimulation, the spikes generally disappear because the membrane now remains entirely depolarized. Figure 35-10 also illustrates the response of smooth muscle fibers to stimulation by norepinephrine or sympathetic excitation. In this situation, the resting membrane potential is decreased, or hyperpolarized, and electrical activity is almost abolished.

In general, most contraction in the GI tract occurs in response to spike potentials; slow waves without superimposed spikes ordinarily do not lead to contraction. Spike potentials occurring in GI smooth muscle are analogous to action potentials in cardiac muscle and are responsible for the membrane changes that initiate contraction. As calcium enters the cell membrane and passes to the interior of the smooth muscle, it initiates a reaction between actin and myosin,1 a process described in detail in Chapter 17.

The electrical activity occurring in the smooth muscle of the gut develops into tonic contractions and rhythmic contractions, both of which occur in most types of smooth muscle. Tonic contraction is continuous, instigated by pacemaker cells that reside at the interface between the longitudinal and circular muscle layers. The intensity of tonic contraction varies with the frequency of spike potentials and determines the amount of pressure in that segment. Thus, the degree of contraction exerted by the pyloric, ileocecal, and anal sphincters serves to regulate the movement of nutrients through the GI tract.

The degree of rhythmic contraction varies in different parts of the GI tract. These differing rhythmic frequencies are dependent on the rate of slow wave activity in a particular segment and may occur at rates of 3 to 12 times per minute. These slow wave–dependent contractions are responsible for the mixing and peristaltic propulsive movements present in the GI tract.

Two types of muscular activity are involved in the digestive and absorptive functions of the GI tract: mixing movements and propulsive movements. In different portions of the GI tract these movements may serve different functions to achieve proper digestion and absorption of nutrients. For example, mixing movements in the stomach and small intestine promote digestion by mixing the digestive juices with the food that enters from the esophagus. In the small intestine and proximal segment of the large intestine, mixing movements facilitate absorption by exposing newly arrived intestinal contents into contact with absorbing surfaces. In the case of propulsion, the rate at which nutrients are propelled through the GI tract depends on the function of the different organs of the tract. For example, the passageway for nutrients from the mouth through the pharynx and esophagus is simply a conduit; essentially no digestive or absorptive function occurs there and the transit of nutrients is quite rapid. In contrast, transit from the stomach and through the small and large intestines is quite slow. This slow rate of passage allows for completion of the digestive and absorptive processes that occur in these portions of the GI tract.

Although the characteristics of mixing and propulsive movements differ in various parts of the GI tract and will be described separately in the next section, a description of the general characteristics of these movements is presented here.

The basic propulsive movement of the GI tract is called peristalsis (Figure 35-11). Nutrients are propelled by the slow advancement of a circular constriction that squeezes the materials in front of the constricted area forward. Peristalsis is an inherent property of any smooth muscle tube that, like the intestine, is a functional syncytium. However, effective intestinal peristalsis requires the presence of an intact myenteric nerve plexus. The usual stimulus for peristalsis is distention of the intestinal walls. The entry and subsequent stretching of the intestinal wall by a bolus of food will have the effect of stimulating the gut wall 2 to 3 cm above this point, and a circular constriction will then occur and propel the food with a peristaltic movement. Although peristalsis can move in both directions in the gut, it normally moves toward the anus. It is thought that the myenteric plexus is organized in such a way that preferential transmission of signals downward occurs simultaneously with relaxation of the distal portion of the intestine below the distended stimulus point.

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