Guyton and Hall Textbook of Medical Physiology, 12th Ed

CHAPTER 66

Physiology of Gastrointestinal Disorders

image Effective therapy for most gastrointestinal disorders depends on a basic knowledge of gastrointestinal physiology. The purpose of this chapter is to discuss a few representative types of gastrointestinal malfunction that have special physiologic bases or consequences.

Disorders of Swallowing and of the Esophagus

Paralysis of the Swallowing Mechanism

Damage to the fifth, ninth, or tenth cerebral nerve can cause paralysis of significant portions of the swallowing mechanism. Also, a few diseases, such as poliomyelitis or encephalitis, can prevent normal swallowing by damaging the swallowing center in the brain stem. Finally, paralysis of the swallowing muscles, as occurs in muscle dystrophy or in failure of neuromuscular transmission in myasthenia gravisor botulism, can also prevent normal swallowing.

When the swallowing mechanism is partially or totally paralyzed, the abnormalities that can occur include (1) complete abrogation of the swallowing act so that swallowing cannot occur, (2) failure of the glottis to close so that food passes into the lungs instead of the esophagus, and (3) failure of the soft palate and uvula to close the posterior nares so that food refluxes into the nose during swallowing.

One of the most serious instances of paralysis of the swallowing mechanism occurs when patients are under deep anesthesia. Often, while on the operating table, they vomit large quantities of materials from the stomach into the pharynx; then, instead of swallowing the materials again, they simply suck them into the trachea because the anesthetic has blocked the reflex mechanism of swallowing. As a result, such patients occasionally choke to death on their own vomitus.

Achalasia and Megaesophagus

Achalasia is a condition in which the lower esophageal sphincter fails to relax during swallowing. As a result, food swallowed into the esophagus then fails to pass from the esophagus into the stomach. Pathological studies have shown damage in the neural network of the myenteric plexus in the lower two thirds of the esophagus. As a result, the musculature of the lower esophagus remains spastically contracted and the myenteric plexus has lost its ability to transmit a signal to cause “receptive relaxation” of the gastroesophageal sphincter as food approaches this sphincter during swallowing.

When achalasia becomes severe, the esophagus often cannot empty the swallowed food into the stomach for many hours, instead of the few seconds that is the normal time. Over months and years, the esophagus becomes tremendously enlarged until it often can hold as much as 1 liter of food, which often becomes putridly infected during the long periods of esophageal stasis. The infection may also cause ulceration of the esophageal mucosa, sometimes leading to severe substernal pain or even rupture and death. Considerable benefit can be achieved by stretching the lower end of the esophagus by means of a balloon inflated on the end of a swallowed esophageal tube. Antispasmotic drugs (drugs that relax smooth muscle) can also be helpful.

Disorders of the Stomach

Gastritis—Inflammation of the Gastric Mucosa

Mild to moderate chronic gastritis is exceedingly common in the population as a whole, especially in the middle to later years of adult life.

The inflammation of gastritis may be only superficial and therefore not very harmful, or it can penetrate deeply into the gastric mucosa, in many long-standing cases causing almost complete atrophy of the gastric mucosa. In a few cases, gastritis can be acute and severe, with ulcerative excoriation of the stomach mucosa by the stomach’s own peptic secretions.

Research suggests that much gastritis is caused by chronic bacterial infection of the gastric mucosa. This often can be treated successfully by an intensive regimen of antibacterial therapy.

In addition, certain ingested irritant substances can be especially damaging to the protective gastric mucosal barrier—that is, to the mucous glands and to the tight epithelial junctions between the gastric lining cells—often leading to severe acute or chronic gastritis. Two of the most common of these substances are excesses of alcohol or aspirin.

Gastric Barrier and Its Penetration in Gastritis

Absorption of food from the stomach directly into the blood is normally slight. This low level of absorption is mainly due to two specific features of the gastric mucosa: (1) It is lined with highly resistant mucous cells that secrete viscid and adherent mucus and (2) it has tight junctions between the adjacent epithelial cells. These two together plus other impediments to gastric absorption are called the “gastric barrier.”

The gastric barrier normally is resistant enough to diffusion so that even the highly concentrated hydrogen ions of the gastric juice, averaging about 100,000 times the concentration of hydrogen ions in plasma, seldom diffuse even to the slightest extent through the lining mucus as far as the epithelial membrane itself. In gastritis, the permeability of the barrier is greatly increased. The hydrogen ions do then diffuse into the stomach epithelium, creating additional havoc and leading to a vicious circle of progressive stomach mucosal damage and atrophy. It also makes the mucosa susceptible to digestion by the peptic digestive enzymes, thus frequently resulting in a gastric ulcer.

Chronic Gastritis Can Lead to Gastric Atrophy and Loss of Stomach Secretions

In many people who have chronic gastritis, the mucosa gradually becomes more and more atrophic until little or no gastric gland digestive secretion remains. It is also believed that some people develop autoimmunity against the gastric mucosa, which also leads eventually to gastric atrophy. Loss of the stomach secretions in gastric atrophy leads to achlorhydria and, occasionally, to pernicious anemia.

Achlorhydria (and Hypochlorhydria)

Achlorhydria means simply that the stomach fails to secrete hydrochloric acid; it is diagnosed when the pH of the gastric secretions fails to decrease below 6.5 after maximal stimulation. Hypochlorhydriameans diminished acid secretion. When acid is not secreted, pepsin also usually is not secreted; even when it is, the lack of acid prevents it from functioning because pepsin requires an acid medium for activity.

Gastric Atrophy May Cause Pernicious Anemia

Pernicious anemia is a common accompaniment of gastric atrophy and achlorhydria. Normal gastric secretions contain a glycoprotein called intrinsic factor, secreted by the same parietal cells that secrete hydrochloric acid. Intrinsic factor must be present for adequate absorption of vitamin B12 from the ileum. That is, intrinsic factor combines with vitamin B12 in the stomach and protects it from being digested and destroyed as it passes into the small intestine. Then, when the intrinsic factor–vitamin B12 complex reaches the terminal ileum, the intrinsic factor binds with receptors on the ileal epithelial surface. This in turn makes it possible for the vitamin B12 to be absorbed.

In the absence of intrinsic factor, only about 1/50 of the vitamin B12 is absorbed. And, without intrinsic factor, an adequate amount of vitamin B12 is not made available from the foods to cause young, newly forming red blood cells to mature in the bone marrow. The result is pernicious anemia. This is discussed in more detail in Chapter 32.

Peptic Ulcer

A peptic ulcer is an excoriated area of stomach or intestinal mucosa caused principally by the digestive action of gastric juice or upper small intestinal secretions. Figure 66-1 shows the points in the gastrointestinal tract at which peptic ulcers most frequently occur, demonstrating that the most frequent site is within a few centimeters of the pylorus. In addition, peptic ulcers frequently occur along the lesser curvature of the antral end of the stomach or, more rarely, in the lower end of the esophagus where stomach juices frequently reflux. A type of peptic ulcer called a marginal ulcer also often occurs wherever a surgical opening such as a gastrojejunostomy has been made between the stomach and the jejunum of the small intestine.

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Figure 66-1 Peptic ulcer. H. pylori, Helicobacter pylori.

Basic Cause of Peptic Ulceration

The usual cause of peptic ulceration is an imbalance between the rate of secretion of gastric juice and the degree of protection afforded by (1) the gastroduodenal mucosal barrier and (2) the neutralization of the gastric acid by duodenal juices. It will be recalled that all areas normally exposed to gastric juice are well supplied with mucous glands, beginning with compound mucous glands in the lower esophagus plus the mucous cell coating of the stomach mucosa, the mucous neck cells of the gastric glands, the deep pyloric glands that secrete mainly mucus, and, finally, the glands of Brunner’s of the upper duodenum, which secrete a highly alkaline mucus.

In addition to the mucus protection of the mucosa, the duodenum is protected by the alkalinity of the small intestinal secretions. Especially important is pancreatic secretion, which contains large quantities of sodium bicarbonate that neutralize the hydrochloric acid of the gastric juice, thus also inactivating pepsin and preventing digestion of the mucosa. In addition, large amounts of bicarbonate ions are provided in (1) the secretions of the large Brunner’s glands in the first few centimeters of the duodenal wall and (2) in bile coming from the liver.

Finally, two feedback control mechanisms normally ensure that this neutralization of gastric juices is complete, as follows:

1. When excess acid enters the duodenum, it inhibits gastric secretion and peristalsis in the stomach, both by nervous reflexes and by hormonal feedback from the duodenum, thereby decreasing the rate of gastric emptying.

2. The presence of acid in the small intestine liberates secretin from the intestinal mucosa, which then passes by way of the blood to the pancreas to promote rapid secretion of pancreatic juice. This juice also contains a high concentration of sodium bicarbonate, thus making still more sodium bicarbonate available for neutralization of the acid.

Therefore, a peptic ulcer can be caused in either of two ways: (1) excess secretion of acid and pepsin by the gastric mucosa or (2) diminished ability of the gastroduodenal mucosal barrier to protect against the digestive properties of the stomach acid–pepsin secretion.

Specific Causes of Peptic Ulcer in the Human Being

Bacterial Infection by Helicobacter pylori Breaks Down the Gastroduodenal Mucosal Barrier and Stimulates Gastric Acid Secretion

At least 75 percent of peptic ulcer patients have been found to have chronic infection of the terminal portions of the gastric mucosa and initial portions of the duodenal mucosa, most often caused by the bacterium Helicobacter pylori.Once this infection begins, it can last a lifetime unless it is eradicated by antibacterial therapy. Furthermore, the bacterium is capable of penetrating the mucosal barrier both by virtue of its physical capability to burrow through the barrier and by releasing ammonium that liquefies the barrier and stimulates the secretion of hydrochloric acid. As a result, the strong acidic digestive juices of the stomach secretions can then penetrate into the underlying epithelium and literally digest the gastrointestinal wall, thus leading to peptic ulceration.

Other Causes of Ulceration

In many people who have peptic ulcers in the initial portion of the duodenum, the rate of gastric acid secretion is greater than normal, sometimes as much as twice normal. Although part of this increased secretion may be stimulated by bacterial infection, studies in both animals and human beings have shown that excess secretion of gastric juices for any reason (for instance, even in psychic disturbances) may cause peptic ulceration.

Other factors that predispose to ulcers include (1) smoking, presumably because of increased nervous stimulation of the stomach secretory glands; (2) alcohol, because it tends to break down the mucosal barrier; and (3) aspirin and other nonsteroidal anti-inflammatory drugs that also have a strong propensity for breaking down this barrier.

Treatment of Peptic Ulcers

Since discovery of the bacterial infectious basis for much peptic ulceration, therapy has changed immensely. Initial reports are that almost all patients with peptic ulceration can be treated effectively by two measures: (1) use of antibiotics along with other agents to kill infectious bacteria and (2) administration of an acid-suppressant drug, especially ranitidine, an antihistaminic that blocks the stimulatory effect of histamine on gastric gland histamine2receptors, thus reducing gastric acid secretion by 70 to 80 percent.

In the past, before these approaches to peptic ulcer therapy were developed, it was often necessary to remove as much as four fifths of the stomach, thus reducing stomach acid–peptic juices enough to cure most patients. Another therapy was to cut the two vagus nerves that supply parasympathetic stimulation to the gastric glands. This blocked almost all secretion of acid and pepsin and often cured the ulcer or ulcers within 1 week after the operation. However, much of the basal stomach secretion returned after a few months and in many patients the ulcer also returned.

The newer physiologic approaches to therapy may prove to be miraculous. Even so, in a few instances, the patient’s condition is so severe, including massive bleeding from the ulcer, that heroic operative procedures often must still be used.

Disorders of the Small Intestine

Abnormal Digestion of Food in the Small Intestine—Pancreatic Failure

A serious cause of abnormal digestion is failure of the pancreas to secrete pancreatic juice into the small intestine. Lack of pancreatic secretion frequently occurs (1) in pancreatitis (which is discussed later), (2) when the pancreatic duct is blocked by a gallstone at the papilla of Vater, or (3) after the head of the pancreas has been removed because of malignancy.

Loss of pancreatic juice means loss of trypsin, chymotrypsin, carboxypolypeptidase, pancreatic amylase, pancreatic lipase, and still a few other digestive enzymes. Without these enzymes, up to 60 percent of the fat entering the small intestine may be unabsorbed, as well as one third to one half of the proteins and carbohydrates. As a result, large portions of the ingested food cannot be used for nutrition and copious, fatty feces are excreted.

Pancreatitis—Inflammation of the Pancreas

Pancreatitis can occur in the form of either acute pancreatitis or chronic pancreatitis.

The most common cause of pancreatitis is drinking excess alcohol, and the second most common cause is blockage of the papilla of Vater by a gallstone; the two together account for more than 90 percent of all cases. When a gallstone blocks the papilla of Vater, this blocks the main secretory duct from the pancreas and the common bile duct. The pancreatic enzymes are then dammed up in the ducts and acini of the pancreas. Eventually, so much trypsinogen accumulates that it overcomes the trypsin inhibitor in the secretions and a small quantity of trypsinogen becomes activated to form trypsin. Once this happens, the trypsin activates still more trypsinogen, as well as chymotrypsinogen and carboxypolypeptidase, resulting in a vicious circle until most of the proteolytic enzymes in the pancreatic ducts and acini become activated. These enzymes rapidly digest large portions of the pancreas, sometimes completely and permanently destroying the ability of the pancreas to secrete digestive enzymes.

Malabsorption by the Small Intestinal Mucosa—Sprue

Occasionally, nutrients are not adequately absorbed from the small intestine even though the food has become well digested. Several diseases can cause decreased absorption by the mucosa; they are often classified together under the general term “sprue.” Malabsorption also can occur when large portions of the small intestine have been removed.

Nontropical Sprue

One type of sprue, called variously idiopathic sprue, celiac disease (in children), or gluten enteropathy, results from the toxic effects of gluten present in certain types of grains, especially wheat and rye. Only some people are susceptible to this effect, but in those who are susceptible, gluten has a direct destructive effect on intestinal enterocytes. In milder forms of the disease, only the microvilli of the absorbing enterocytes on the villi are destroyed, thus decreasing the absorptive surface area as much as twofold. In the more severe forms, the villi themselves become blunted or disappear altogether, thus still further reducing the absorptive area of the gut. Removal of wheat and rye flour from the diet frequently results in cure within weeks, especially in children with this disease.

Tropical Sprue

A different type of sprue called tropical sprue frequently occurs in the tropics and can often be treated with antibacterial agents. Even though no specific bacterium has been implicated as the cause, it is believed that this variety of sprue is usually caused by inflammation of the intestinal mucosa resulting from unidentified infectious agents.

Malabsorption in Sprue

In the early stages of sprue, intestinal absorption of fat is more impaired than absorption of other digestive products. The fat that appears in the stools is almost entirely in the form of salts of fatty acids rather than undigested fat, demonstrating that the problem is one of absorption, not of digestion. In fact, the condition is frequently called steatorrhea, which means simply excess fats in the stools.

In severe cases of sprue, in addition to malabsorption of fats there is also impaired absorption of proteins, carbohydrates, calcium, vitamin K, folic acid, and vitamin B12. As a result, the person suffers (1) severe nutritional deficiency, often developing wasting of the body; (2) osteomalacia (demineralization of the bones because of lack of calcium); (3) inadequate blood coagulation caused by lack of vitamin K; and (4) macrocytic anemia of the pernicious anemia type, owing to diminished vitamin B12 and folic acid absorption.

Disorders of the Large Intestine

Constipation

Constipation means slow movement of feces through the large intestine; it is often associated with large quantities of dry, hard feces in the descending colon that accumulate because of overabsorption of fluid. Any pathology of the intestines that obstructs movement of intestinal contents, such as tumors, adhesions that constrict the intestines, or ulcers, can cause constipation. A frequent functional cause of constipation is irregular bowel habits that have developed through a lifetime of inhibition of the normal defecation reflexes.

Infants are seldom constipated, but part of their training in the early years of life requires that they learn to control defecation; this control is effected by inhibiting the natural defecation reflexes. Clinical experience shows that if one does not allow defecation to occur when the defecation reflexes are excited or if one overuses laxatives to take the place of natural bowel function, the reflexes themselves become progressively less strong over months or years, and the colon becomes atonic. For this reason, if a person establishes regular bowel habits early in life, defecating when the gastrocolic and duodenocolic reflexes cause mass movements in the large intestine, the development of constipation in later life is much less likely.

Constipation can also result from spasm of a small segment of the sigmoid colon. It should be recalled that motility normally is weak in the large intestine, so even a slight degree of spasm is often capable of causing serious constipation. After the constipation has continued for several days and excess feces have accumulated above a spastic sigmoid colon, excessive colonic secretions often then lead to a day or so of diarrhea. After this, the cycle begins again, with repeated bouts of alternating constipation and diarrhea.

Megacolon (Hirschsprung’s Disease)

Occasionally, constipation is so severe that bowel movements occur only once every several days or sometimes only once a week. This allows tremendous quantities of fecal matter to accumulate in the colon, causing the colon sometimes to distend to a diameter of 3 to 4 inches. The condition is called megacolon, or Hirschsprung’s disease.

A frequent cause of megacolon is lack of or deficiency of ganglion cells in the myenteric plexus in a segment of the sigmoid colon. As a consequence, neither defecation reflexes nor strong peristaltic motility can occur in this area of the large intestine. The sigmoid itself becomes small and almost spastic while feces accumulate proximal to this area, causing megacolon in the ascending, transverse, and descending colons.

Diarrhea

Diarrhea results from rapid movement of fecal matter through the large intestine. Several causes of diarrhea with important physiologic sequelae are the following.

Enteritis—Inflammation of the Intestinal Tract

Enteritis means inflammation usually caused either by a virus or by bacteria in the intestinal tract. In usual infectious diarrhea, the infection is most extensive in the large intestine and the distal end of the ileum. Everywhere the infection is present, the mucosa becomes irritated and its rate of secretion becomes greatly enhanced. In addition, motility of the intestinal wall usually increases manifold. As a result, large quantities of fluid are made available for washing the infectious agent toward the anus, and at the same time strong propulsive movements propel this fluid forward. This is an important mechanism for ridding the intestinal tract of a debilitating infection.

Of special interest is diarrhea caused by cholera (and less often by other bacteria such as some pathogenic colon bacilli). As explained in Chapter 65, cholera toxin directly stimulates excessive secretion of electrolytes and fluid from the crypts of Lieberkühn in the distal ileum and colon. The amount can be 10 to 12 liters per day, although the colon can usually reabsorb a maximum of only 6 to 8 liters per day. Therefore, loss of fluid and electrolytes can be so debilitating within several days that death can ensue.

The most important physiologic basis of therapy in cholera is to replace the fluid and electrolytes as rapidly as they are lost, mainly by giving the patient intravenous solutions. With proper therapy, along with the use of antibiotics, almost no cholera patients die but without therapy up to 50 percent do.

Psychogenic Diarrhea

Everyone is familiar with the diarrhea that accompanies periods of nervous tension, such as during examination time or when a soldier is about to go into battle. This type of diarrhea, called psychogenicemotional diarrhea, is caused by excessive stimulation of the parasympathetic nervous system, which greatly excites both (1) motility and (2) excess secretion of mucus in the distal colon. These two effects added together can cause marked diarrhea.

Ulcerative Colitis

Ulcerative colitis is a disease in which extensive areas of the walls of the large intestine become inflamed and ulcerated. The motility of the ulcerated colon is often so great that mass movements occur much of the day rather than for the usual 10 to 30 minutes. Also, the colon’s secretions are greatly enhanced. As a result, the patient has repeated diarrheal bowel movements.

The cause of ulcerative colitis is unknown. Some clinicians believe that it results from an allergic or immune destructive effect, but it also could result from chronic bacterial infection not yet understood. Whatever the cause, there is a strong hereditary tendency for susceptibility to ulcerative colitis. Once the condition has progressed far, the ulcers seldom will heal until an ileostomy is performed to allow the small intestinal contents to drain to the exterior rather than to pass through the colon. Even then the ulcers sometimes fail to heal, and the only solution might be surgical removal of the entire colon.

Paralysis of Defecation in Spinal Cord Injuries

From Chapter 63 it will be recalled that defecation is normally initiated by accumulating feces in the rectum, which causes a spinal cord–mediated defecation reflex passing from the rectum to the conus medullaris of the spinal cord and then back to the descending colon, sigmoid, rectum, and anus.

When the spinal cord is injured somewhere between the conus medullaris and the brain, the voluntary portion of the defecation act is blocked while the basic cord reflex for defecation is still intact. Nevertheless, loss of the voluntary aid to defecation—that is, loss of the increased abdominal pressure and relaxation of the voluntary anal sphincter—often makes defecation a difficult process in the person with this type of upper cord injury. But because the cord defecation reflex can still occur, a small enema to excite action of this cord reflex, usually given in the morning shortly after a meal, can often cause adequate defecation. In this way, people with spinal cord injuries that do not destroy the conus medullaris of the spinal cord can usually control their bowel movements each day.

General Disorders of the Gastrointestinal Tract

Vomiting

Vomiting is the means by which the upper gastrointestinal tract rids itself of its contents when almost any part of the upper tract becomes excessively irritated, overdistended, or even overexcitable. Excessive distention or irritation of the duodenum provides an especially strong stimulus for vomiting.

The sensory signals that initiate vomiting originate mainly from the pharynx, esophagus, stomach, and upper portions of the small intestines. And the nerve impulses are transmitted, as shown in Figure 66-2, by both vagal and sympathetic afferent nerve fibers to multiple distributed nuclei in the brain stem that all together are called the “vomiting center.” From here, motor impulses that cause the actual vomiting are transmitted from the vomiting center by way of the fifth, seventh, ninth, tenth, and twelfth cranial nerves to the upper gastrointestinal tract, through vagal and sympathetic nerves to the lower tract, and through spinal nerves to the diaphragm and abdominal muscles.

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Figure 66-2 Neutral connections of the “vomiting center.” This so-called vomiting center includes multiple sensory, motor, and control nuclei mainly in the medullary and pontile reticular formation but also extending into the spinal cord.

Antiperistalsis, the Prelude to Vomiting

In the early stages of excessive gastrointestinal irritation or overdistention, antiperistalsis begins to occur often many minutes before vomiting appears. Antiperistalsis means peristalsis up the digestive tract rather than downward. This may begin as far down in the intestinal tract as the ileum, and the antiperistaltic wave travels backward up the intestine at a rate of 2 to 3 cm/sec; this process can actually push a large share of the lower small intestine contents all the way back to the duodenum and stomach within 3 to 5 minutes. Then, as these upper portions of the gastrointestinal tract, especially the duodenum, become overly distended, this distention becomes the exciting factor that initiates the actual vomiting act.

At the onset of vomiting, strong intrinsic contractions occur in both the duodenum and the stomach, along with partial relaxation of the esophageal-stomach sphincter, thus allowing vomitus to begin moving from the stomach into the esophagus. From here, a specific vomiting act involving the abdominal muscles takes over and expels the vomitus to the exterior, as explained in the next paragraph.

Vomiting Act

Once the vomiting center has been sufficiently stimulated and the vomiting act instituted, the first effects are (1) a deep breath, (2) raising of the hyoid bone and larynx to pull the upper esophageal sphincter open, (3) closing of the glottis to prevent vomitus flow into the lungs, and (4) lifting of the soft palate to close the posterior nares. Next comes a strong downward contraction of the diaphragm along with simultaneous contraction of all the abdominal wall muscles. This squeezes the stomach between the diaphragm and the abdominal muscles, building the intragastric pressure to a high level. Finally, the lower esophageal sphincter relaxes completely, allowing expulsion of the gastric contents upward through the esophagus.

Thus, the vomiting act results from a squeezing action of the muscles of the abdomen associated with simultaneous contraction of the stomach wall and opening of the esophageal sphincters so that the gastric contents can be expelled.

“Chemoreceptor Trigger Zone” in the Brain Medulla for Initiation of Vomiting by Drugs or by Motion Sickness

Aside from the vomiting initiated by irritative stimuli in the gastrointestinal tract, vomiting can also be caused by nervous signals arising in areas of the brain. This is particularly true for a small area located bilaterally on the floor of the fourth ventricle called the chemoreceptor trigger zone for vomiting. Electrical stimulation of this area can initiate vomiting; but, more important, administration of certain drugs, including apomorphine, morphine, and some digitalis derivatives, can directly stimulate this chemoreceptor trigger zone and initiate vomiting. Destruction of this area blocks this type of vomiting but does not block vomiting resulting from irritative stimuli in the gastrointestinal tract itself.

Also, it is well known that rapidly changing direction or rhythm of motion of the body can cause certain people to vomit. The mechanism for this is the following: The motion stimulates receptors in the vestibular labyrinth of the inner ear, and from here impulses are transmitted mainly by way of the brain stem vestibular nuclei into the cerebellum, then to the chemoreceptor trigger zone, and finally to the vomiting center to cause vomiting.

Nausea

Everyone has experienced the sensation of nausea and knows that it is often a prodrome of vomiting. Nausea is the conscious recognition of subconscious excitation in an area of the medulla closely associated with or part of the vomiting center, and it can be caused by (1) irritative impulses coming from the gastrointestinal tract, (2) impulses that originate in the lower brain associated with motion sickness, or (3) impulses from the cerebral cortex to initiate vomiting. Vomiting occasionally occurs without the prodromal sensation of nausea, indicating that only certain portions of the vomiting center are associated with the sensation of nausea.

Gastrointestinal Obstruction

The gastrointestinal tract can become obstructed at almost any point along its course, as shown in Figure 66-3. Some common causes of obstruction are (1) cancer, (2) fibrotic constriction resulting from ulceration or from peritoneal adhesions, (3) spasm of a segment of the gut, and (4) paralysis of a segment of the gut.

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Figure 66-3 Obstruction in different parts of the gastrointestinal tract.

The abnormal consequences of obstruction depend on the point in the gastrointestinal tract that becomes obstructed. If the obstruction occurs at the pylorus, which results often from fibrotic constriction after peptic ulceration, persistent vomiting of stomach contents occurs. This depresses bodily nutrition; it also causes excessive loss of hydrogen ions from the stomach and can result in various degrees of whole-body metabolic alkalosis.

If the obstruction is beyond the stomach, antiperistaltic reflux from the small intestine causes intestinal juices to flow backward into the stomach, and these juices are vomited along with the stomach secretions. In this instance, the person loses large amounts of water and electrolytes. He or she becomes severely dehydrated, but the loss of acid from the stomach and base from the small intestine may be approximately equal, so little change in acid-base balance occurs.

If the obstruction is near the distal end of the large intestine, feces can accumulate in the colon for a week or more. The patient develops an intense feeling of constipation, but at first vomiting is not severe. After the large intestine has become completely filled and it finally becomes impossible for additional chyme to move from the small intestine into the large intestine, severe vomiting does then occur. Prolonged obstruction of the large intestine can finally cause rupture of the intestine itself or dehydration and circulatory shock resulting from the severe vomiting.

Gases in the Gastrointestinal Tract; “Flatus”

Gases, called flatus, can enter the gastrointestinal tract from three sources: (1) swallowed air, (2) gases formed in the gut as a result of bacterial action, or (3) gases that diffuse from the blood into the gastrointestinal tract. Most gases in the stomach are mixtures of nitrogen and oxygen derived from swallowed air. In the typical person these gases are expelled by belching. Only small amounts of gas normally occur in the small intestine, and much of this gas is air that passes from the stomach into the intestinal tract.

In the large intestine, most of the gases are derived from bacterial action, including especially carbon dioxide, methane, and hydrogen. When methane and hydrogen become suitably mixed with oxygen, an actual explosive mixture is sometimes formed. Use of the electric cautery during sigmoidoscopy has been known to cause a mild explosion.

Certain foods are known to cause greater expulsion of flatus through the anus than others—beans, cabbage, onion, cauliflower, corn, and certain irritant foods such as vinegar. Some of these foods serve as a suitable medium for gas-forming bacteria, especially unabsorbed fermentable types of carbohydrates. For instance, beans contain an indigestible carbohydrate that passes into the colon and becomes a superior food for colonic bacteria. But in other instances, excess expulsion of gas results from irritation of the large intestine, which promotes rapid peristaltic expulsion of gases through the anus before they can be absorbed.

The amount of gases entering or forming in the large intestine each day averages 7 to 10 liters, whereas the average amount expelled through the anus is usually only about 0.6 liter. The remainder is normally absorbed into the blood through the intestinal mucosa and expelled through the lungs.

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