any of the diseases that affect the human digestive tract. They include infections, inflammations, ulcers, and cancers. Additional reading Gastrointestinal diseases are treated in such works as Charles H. Best, Best and Taylor's Physiological Basis of Medical Practice, 11th ed., edited by John B. West (1985); and E.J. Holborow and W.G. Reeves (eds.), Immunology in Medicine: A Comprehensive Guide to Clinical Immunology, 2nd ed. (1983). Specialized studies include Harvey J. Dworken, Gastroenterology: Pathophysiology and Clinical Applications (1982); Marvin H. Sleisenger and John S. Fordtran (eds.), Gastrointestinal Disease: Pathophysiology, Diagnosis, Management, 3rd ed. (1983); David J.C. Shearman and Niall D.C. Finlayson, Diseases of the Gastrointestinal Tract and Liver (1982); H.L. Duthie (ed.), Gastrointestinal Motility in Health and Disease (1978); F. Avery Jones, J.W.P. Gummer, and J.E. Lennard-Jones, Clinical Gastroenterology, 2nd ed. (1968); Moses Paulson (ed.), Gastroenterologic Medicine (1969); Henry L. Bockus, Bockus Gastroenterology, 4th ed., edited by J. Edward Berk et al., 7 vol. (1985); and Brian M. Barker and David A. Bender (eds.), Vitamins in Medicine, 4th ed., 2 vol. (198082). For current research in the field, see Gastroenterology Annual. Biliary tract Gallstones Cholelithiasis, or the formation of gallstones in the gallbladder, is the most common disease of the biliary tract. Gallstones are of three types: stones containing primarily calcium bilirubinate (pigment stones); stones containing 25 percent or more of cholesterol; and stones composed of variable mixtures of both bilirubin and cholesterol (mixed gallstones). Purely pigment stones are more common in certain parts of Asia than in the West, and they are prone to occur in persons who suffer from forms of anemia caused by the rapid destruction of red blood cells (hemolysis). Hemolytic disease results from the hereditary or acquired acquisition of abnormal forms of hemoglobin or from abnormalities of the red blood cell membrane in disorders such as sickle-cell anemia, thalassemia, or acquired hemolytic anemias. Increased destruction of red blood cells leads to abnormally large amounts of bilirubin, the hemoglobin derivative, in the liver and the consequent secretion into the biliary tract of increased amounts of the water-soluble conjugate, bilirubin diglucuronide, a pigment that is normally secreted in the urine. In the biliary tract, particularly in the gallbladder, some of this bilirubin diglucuronide is broken down by bacterial or mucosal enzymes into water-insoluble bilirubin, which then tends to form stones. There are two types of pigment stones, black and brown. Black stones tend to form mainly in the gallbladder and occur in sterile bile, while brown stones may occur in any part of the biliary tract in patients with chronic biliary infections and varying degrees of stasis. The reasons for the increased incidence of pigment stones among persons with cirrhosis of the liver and the aged are not clear, although increased red blood cell destruction may play a part. The occurrence of pigment stones is slightly more common in women. Cholesterol and mixed cholesterol-bilirubinate stones occur when the proportion of cholesterol in bile exceeds the capacity of bile acids and lecithin to contain the total amount of cholesterol in micellar colloidal solution. When this critical micellar concentration is surpassed and the solution is saturated, crystalline particles of cholesterol are formed. The resulting gallstones contain large amounts of crystalline cholesterol and smaller quantities of calcium bilirubinate. Pure cholesterol gallstones are rare. Cholesterol gallstones occur about twice as frequently in women as they do in men, and at younger ages. Those at increased risk of cholesterol gallstones include persons who are obese, on diets high in caloric content or in cholesterol, diabetic, or taking female sex hormones. Each of these factors favours increased concentrations of cholesterol in bile. In addition, some persons are unable, for genetic reasons, to convert sufficient amounts of cholesterol to bile acids, thus favouring the increased formation of stones. Some illnesses reduce the capacity of the lower small intestine to reabsorb bile acids, leading to deficits of bile acids that cannot be overcome by hepatic synthesis alone. During pregnancy, the ratio of chenodeoxycholic acid to cholic acid in hepatic bile is reduced, thus making bile more prone to produce stones (lithogenic). Decreased flow of bile in the gallbladder, a condition that occurs late in pregnancy, in persons on diets low in fat, and among certain diabetics, also appears to favour the formation of cholesterol stones. Occasionally, some persons produce lithogenic bile, which results from reduced concentrations of phospholipids. Symptoms are likely to be absent in about half of all patients who have gallstones. When they do appear, symptoms are caused by transient or prolonged obstruction of a portion of the biliary tract, most commonly the cystic duct at the point where it emerges from the gallbladder. This obstruction leads to painful contraction of the gallbladder, swelling of its wall, and acute inflammation (cholecystitis). During an attack of cholecystitis, patients are often found to have fever, sharp pain in the abdomen (which also may be felt in the right shoulder region), tenderness over the region of the gallbladder, and elevations of the white blood cell count. If the obstruction of the neck of the gallbladder is prolonged, bacterial infections may appear, leading to formation of an abscess. Patients with bacterial infections in the gallbladder or bile ducts commonly have severe rigours, or shaking chills, with high, spiking fevers. Jaundice does not occur with gallstone complications unless the stones become impacted and obstruct the common bile duct, thus slowing or interrupting the free passage of bile from the liver to the intestine. This jaundice is associated with a marked lightening of stool colour, caused by the absence of bile pigments in the intestine, and a change in the colour of urine to a dark amber, caused by large quantities of conjugated bilirubin. Gallstone disease is easy to diagnose since calculi in the gallbladder can be easily detected by ultrasonography. Enlargement of the gallbladder and bile ducts (resulting from obstruction) also can be detected by this method. As many as one-half of all persons with gallstones never have serious symptoms or complications. Thus, if gallstones are discovered on routine examination or during abdominal surgery for other reasons, and if the patient has no history of gallstone symptoms, nothing probably needs to be done. The situation is different, however, in persons who are clearly symptomatic or who are suffering acute complications, such as cholecystitis or abscesses. The traditional treatment in these cases is surgical removal of the diseased gallbladder and exploration of the bile ducts by X rays at the time of surgery for stones. The risks of this surgery are extremely small, although they do increase considerably in persons with acute complications and in older persons. Once the gallbladder and ductal stones are removed, there is little likelihood that cholesterol or black pigment stones will recur, although brown pigment stones may occasionally recur in the bile ducts after cholecystectomy. Many cholesterol gallstones can be dissolved without surgery as long as the gallbladder has retained its ability to concentrate bile and the cystic duct is unobstructed. This is accomplished by regular oral administration of the bile acids chenodeoxycholic acid or ursodeoxycholic acid. The ingestion of these acids increases the amount of bile acids in hepatic bile and increases the ratio of bile acids to cholesterol, thus changing the bile from lithogenic to nonlithogenic. This medication must be continued for more than one year for the cholesterol gallstones to be completely dissolved and then continued permanently at reduced doses to prevent the reappearance of stones. Only a small percentage of patients are willing to undergo this permanent treatment, and the use of bile acids is confined either to those who strongly oppose surgery or those for whom surgery imposes great risk. Pigment stones do not respond to bile acid therapy. Other biliary tract disorders Cancer of the biliary tract is rare but may occur in almost any area, including the gallbladder, the hepatic ducts, the common bile duct, or the ampulla of Vater. About 90 percent of persons with primary cancer of the gallbladder also have gallstones. The risk of cancer in persons with gallstones, however, is very low (about 1 percent or less). In cancer of the bile duct, congenital cysts and parasitic infections, such as liver flukes, seem to lead to increased risks. Persons with extensive chronic ulcerative colitis also show a greater than normal incidence of bile duct carcinoma. Obstructive jaundice is usually the first sign of biliary tract cancer. Surgery is the only treatment, and the chances of cure are very small. Because most biliary duct cancers grow very slowly, physicians often try to relieve the obstructive jaundice by passing tubular stents (supporting devices) through the obstruction, using endoscopic or radiologic techniques. Postcholecystectomy syndrome comprises painful attacks, often resembling preoperative symptoms, that occasionally occur following the surgical removal of gallstones and the gallbladder. These attacks may be related to intermittent muscular spasms of the sphincter of Oddi or of the bile ducts. Drugs are used to help prevent or reduce these spasms. Large intestine A wide variety of diseases and disorders occur in the large intestine. Imperfect fetal development may result in an anus that has no opening, a defect that requires major plastic surgery to correct. Abnormal rotation of the colon is fairly frequent and occasionally leads to disorders. Unusually long mesenteries (the supporting tissues of the large intestine) may permit recurrent twisting, cutting off the blood supply to the involved loop. The loop itself may be completely obstructed by rotation. Such complications are usually seen in elderly patients and particularly in those with a long history of constipation. Simple constipation Brain disease, metabolic failure, or drugs can dull the normal signals that give rise to the urge to defecate. Poor abdominal musculature or a poor pelvic floor, sometimes the result of surgery or childbirth, makes it difficult to mobilize effective pressures to bring about defecation. Liver A variety of agents, including viruses, drugs, environmental pollutants, genetic disorders, and systemic diseases, can affect the liver. The resulting disorders usually affect one of the three functional components of the liver: the hepatocyte (liver cell) itself, the bile secretory (cholangiolar) apparatus, or the blood vascular system. Although an agent tends to cause initial damage in only one of these areas, the resulting disease may in time also involve other components. Thus, although viral hepatitis (inflammation of the liver) predominantly affects hepatocytes, it commonly leads eventually to canalicular damage. Most acute liver diseases are self-limited, and liver functioning returns to normal once the causes are removed or eliminated. In some cases, however, the acute disease process destroys massive areas of liver tissue in a short time, leading to extensive death (necrosis) of hepatic cells and often to death of the patient. Hepatitis may result from viral infections or toxic damage from drugs or poisons. When acute hepatitis lasts for six months or more, a slow but progressive destruction of the surrounding liver cells and bile ducts occurs, a stage called chronic active hepatitis. If hepatocellular damage is severe enough to destroy entire acini (clusters of lobules), they are often replaced with fibrous scar tissue. Bile canaliculi and hepatocytes regenerate in an irregular fashion adjacent to the scar tissue and result in a chronic condition called cirrhosis of the liver. Where inflammatory activity continues after the onset of cirrhosis, the disorderly regeneration of hepatocytes and cholangioles may lead to the development of hepatocellular or cholangiolar cancer. Acute hepatocellular hepatitis Although a number of viruses affect the liver, including the cytomegalovirus of infancy and childhood and the Epstein-Barr virus of infectious mononucleosis, there are three distinctive transmissible viruses that are specifically known to cause acute damage to liver cells: hepatitis virus A (HAV), hepatitis virus B (HBV), and hepatitis virus non-A, non-B (NANB). The hepatitis A virus is transmitted almost exclusively by the fecaloral route, and it thrives in areas where sanitation and food handling are poor and hand washing is infrequent. Hepatitis A virus proliferates in the intestinal tract during the two weeks following the onset of symptoms, but it then disappears. Many infected persons are unaware of being ill, since their disease remains asymptomatic or quite mild. The incubation period of HAV infections, from viral ingestion to the onset of symptoms, averages four to five weeks. Acute illness in an otherwise healthy pregnant woman does not appear to have adverse effects upon the fetus. Persons can become passively immunized against hepatitis A attacks for several months with a single injection of immunoglobulin, a product made from pools of 100 or more donor plasmas. Persons can be actively immunized to HAV by acquiring the virus subsequent to becoming passively immunized, but such infections are either inapparent or very mild. An active vaccine is not available, and there are no carriers of the virus. Hepatitis B virus is present throughout the world in asymptomatic human carriers who may or may not have ongoing liver disease. Formerly, the disease was widely spread by the transfusion of whole blood or blood products, such as the cryoprecipitate used in the treatment of hemophilia. Since the markers of infection have become so readily identifiable, this mode of transmission is much less common, comprising only about 10 percent of cases, compared with 60 percent in the past. Hepatitis B virus is still transmitted in some blood specimens because the levels of virus particles present may be too low to be detected. Virus particles in carriers are found in bodily secretions, especially saliva and sexual emissions, as well as in blood. The incidence of B antigens is high among persons engaging in promiscuous sexual activity, drug addicts who share syringes, health care workers, and infants of mothers who are carriers. Many newly infected persons develop the acute disease within three weeks to six months after exposure, while some develop an asymptomatic form of hepatitis that may appear only as chronic disease years later. Others eliminate the virus completely without any symptoms beyond the appearance of antibodies to surface antigen, while still others become carriers of surface antigen and thus presumably are infective to others. There are two methods of preventing hepatitis B: passive immunization, through the use of a specific immunoglobulin derived from patients who have successfully overcome an acute HBV infection; and active immunization, through the injection of noninfective, purified HBV surface antigen. The first method is used following specific exposures that carry a high risk of infection, such as using needles contaminated with HBV particles, the ingestion of body products likely to be infected, or the birth of an infant to a surface-antigen-positive mother. The second method, active immunization, is used for those who belong to groups with a high risk of HBV infection, such as children living in endemic areas, medical personnel in high-risk specialties, drug addicts, sexually promiscuous persons, and family groups living close to known carriers. Active immunization, involving a series of three injections of vaccine over a period of three to six months, has been shown to confer a high degree of resistance to infection. Non-A, non-B hepatitis virus has not been isolated, so that the markers of infection and of immunity are not available. Because of this, NANB is the major cause of posttransfusion hepatitis, and it appears with a frequency of three to six cases per 1,000 transfusions of blood prescreened for HBV. The average incubation period of the disease is about seven weeks, and an acute attack of NANB hepatitis is usually less severe than acute hepatitis B. Non-A, non-B hepatitis, however, is more likely to become chronic than is hepatitis B, and it may recur episodically with acute flares. The symptoms characteristic of the acute hepatitis caused by the HAV, HBV, and NANB viruses are essentially indistinguishable from one another. Patients often complain of a flulike illness for several days, with chills, variable degrees of fever, headache, cough, nausea, occasional diarrhea, and pronounced malaise. Abdominal pain caused by swelling of the liver is a common complaint. As many as half of the infected patients develop only mild symptoms or none at all. A small percentage of patients, especially those with HBV infections, may develop hives, painful skin nodules, acute arthritis, or urinary bleeding caused by the deposition of large immune antigenantibody complexes in the small blood vessels of adjacent organs. After several days or a week of such symptoms, jaundice commonly develops. At times the jaundice is so mild that it is not noticed by patients, although they often do note that the urine has become dark amber in colour because of the high levels of water-soluble bilirubin transmitted to the kidneys by the bloodstream. The onset of jaundice usually brings with it a marked improvement in other symptoms (see below, Biliary tract: Jaundice). Jaundice lasts about two weeks but may continue for several months, even in those who have complete recovery. Some patients complain of itching during this period, and they notice the light colour of their stools. These symptoms probably result from the compression of bile canaliculi and intralobular bile ducts by the swelling of hepatocytes and Kupffer cells. The changes result in the reduced secretion of bile pigments into the biliary system, their reflux into the bloodstream, and the deposition of bile salts and other biliary constituents in the skin and subcutaneous tissues, a condition called obstructive jaundice. After the phase of jaundice subsides, almost all patients with hepatitis A, and at least 90 percent of those with hepatitis B, recover completely. Aside from jaundice, the physical examination of patients with acute viral hepatitis may reveal nothing more than the swelling of lymph nodes in the neck. Many patients have detectable enlargement and, at times, tenderness of the liver. Some also show an enlarged spleen. Signs of confusion or disorientation indicate severe damage to the liver. The diagnosis of hepatitis is confirmed by blood tests that show marked elevations of enzymes (aminotransferases) released from damaged liver cells and, at times, by the presence of viral antigens or acute viral antibodies (IgM). A small number, perhaps 1 percent, of patients with viral hepatitis, especially the elderly, develop a sudden, severe (fulminant) form of hepatic necrosis that can lead to death. In this form of the disease jaundice increases to high levels during the first seven to 10 days, spontaneous bleeding occurs because of reductions of blood-clotting proteins, and irrational behaviour, confusion, or coma follow, caused by the accumulation in the central nervous system of the breakdown products of protein normally metabolized by the liver. Beyond supportive measures there is no effective treatment of fulminant hepatic failure. Acute hepatitis also may be caused by the overconsumption of alcohol or other poisons, such as commercial solvents (e.g., carbon tetrachloride), acetaminophen, and certain fungi. Such agents are believed to cause hepatitis when the formation of their toxic intermediate metabolites in the liver cell (phase I reactions) is beyond the capacity of the hepatocyte to conjugate, or join them with another substance for detoxification (phase II reactions) and excretion. As long as the levels of these agents are small enough to permit complete phase I and phase II reactions, there is no damage to the liver cell. Mouth and oral cavity Besides local disease, features characteristic of systemic disorders are often present on the mouth and in the oral cavity. The lips may be fissured and eroded at the corners in riboflavin deficiency (angular chelitis). Multiple brown freckles on the lips associated with polyps in the small intestine is characteristic of Peutz-Jegher's syndrome. Spider nevi, which are prominent in chronic liver disease, are not confined to the face or congregated on the lip margins. Aggregates of small yellow spots on the buccal mucosa and the mucosa behind the lips indicate Fordyce's disease. The spots are due to the presence of enlarged sebaceous glands just below the mucosal surface. The most common mouth ulcers are due to aphthous stomatitis. These affect one out of every five Caucasians. The spectrum of this condition ranges from one or two small painful vesicles rupturing to form round or oval ulcers, occurring once or twice a year and lasting seven to 10 days, to deep ulcers of one centimetre or more in diameter. The ulcers are frequently multiple, occur anywhere in the mouth (on the tongue or the palate), and may persist for months at a time. The disability ranges from a mild local irritation to severe distressing pain that prevents talking and eating. Scarring can be seen at the sites of previous ulcers. Aphthous ulceration is sometimes associated with psychological stress, but it may also be a reflection of an underlying malabsorptive disease such as celiac disease. Treatment is directed to the predisposing cause. Local anesthetic agents and analgesics may permit talking and eating. Topical and systemic corticosteroids are the most effective treatment. In a more serious condition, Behet's syndrome, similar ulcers occur in the mouth and on the genitalia, and the eyes are involved. Discoloration of the tongue, commonly white, is due to deposits of epithelial debris, effete (or worn out) bacteria, and food. It occurs in circumstances in which there is reduced saliva production. This may be acute, as in fevers, when the body temperature is high and loss of water through the skin is excessive. The reduced saliva flow in fever is a conservation phenomenon, akin to oliguria (reduced urine losses) and constipation. The discoloration becomes chronic following atrophy of the glands and in the absence of good oral hygiene. If the person is a heavy smoker, the deposit is coloured brown. Black discoloration of the tongue with the formation in the centre of a dense pellicle of fur (black hairy tongue) may be due to a fungus with pigmented filaments. Occasionally it simply represents excessive elongation of the filiform papillae. It may be due to sucking licorice candy. A bald tongue, with a smooth surface due to complete atrophy of the papillae, is seen in severe iron-deficiency anemia, pernicious anemia, and pellagra, a disorder of skin and mucous membranes due to niacin deficiency. This condition occurs in cereal eaters, usually of corn, when the cereal is contaminated or has a low content of the vitamin that leads to an imbalance in the amino acids derived from food. The condition is endemic in underdeveloped countries in which there are periods of famine. A deeply fissured tongue (scrotal tongue) may be due to a congenital variation in the supporting tissue of the tongue, but it can be acquired. There is a mild degree of inflammation in the fissures, which causes a slight burning discomfort. Geographic tongue, or migrating exfoliative glossitis, describes areas of denudation of the surface of the tongue of various shapes and sizes. These gradually become re-epithelialized with regrowth of the filiform papillae, only for the inflammatory process to begin elsewhere in the tongue. Thus, the picture changes with time as the bald zones move around the tongue. These changes usually give rise to no symptoms or, at the most, to a mild burning sensation. The cause is unknown, and the condition may persist for years. Vincent's disease (trench mouth) is an ulcerating, necrotizing infection of the gingiva (gums) notable for the spontaneous bleeding from affected areas and the foul odour of the breath arising from the gangrenous tissue. It is endemic in countries where there is severe malnutrition and poor oral hygiene. The infection probably involves several organisms, including spirochetes and fusiform bacilli. It is uncertain if in the developed countries it is transmitted by the exchange of saliva in kissing, but its epidemic increase in wartime and its frequency in the promiscuous suggest this. Vincent's disease responds to antibiotics followed by trimming of the gum margins to eliminate subgingival pockets. Malignant disease, or cancer, of the mouth is sometimes caused by chronic thermal irritation in heavy smokers and is often preceded by leukoplakia (plaque-like patches arising on the mucous membranes of the cheeks, gum, or tongue). Similarly, cancer of the mouth can be caused by the habit of keeping tobacco or a package of intensely hot spices in the space between the cheek and the teeth. These cancers arise from the squamous cells that line the oral mucosa. Cancers of the salivary glands and of the mucous membranes of the cheeks cause pain, bleeding, or difficulty in swallowing. The lymphomas and other tumours of lymphoid origin may first appear in the tonsillar or pharyngeal lymph nodes. Cancer of the tongue and of the bony structures of the hard palate or sinuses may project into the mouth or may burrow deep into the surrounding tissues. Dental caries Dental caries are due to the destruction of the dental enamel and underlying tissues by organic acids. These acids are formed by bacteria growing in debris and food accumulated in pockets between the base of the teeth and the gum margins. This periodontal infection ultimately leads to the invasion of the dental pulp, and the involvement of the nerve in the inflammation is the cause of toothache. An abscess may form at the apex of the tooth and extend into the jawbone, causing osteomyelitis (inflammation of the bone), or into the soft tissues around the roots of the teeth, causing cellulitis (inflammation of the soft tissues). Halitosis is due to the rotting debris in the pockets under the gum margins. In due course the teeth loosen and fall out or need to be extracted. Poor oral hygiene is the underlying predisposing circumstance. Malnutrition due to poverty, alcoholism, and malabsorption of vitamin D (rickets) or of proteins (as in celiac disease), initiate or aggravate caries. The resistance of the dental enamel to damage by organic acids is increased by fluoride, and in many countries this is incorporated into the toothpaste formula and is added to the water supplied to homes. In areas where these steps have been taken, the incidence of caries has dropped by more than 50 percent. Pancreas Pancreatitis Inflammation of the pancreas, or pancreatitis, is probably the most common disease of this organ. The disorder may be confined to either singular or repeated acute episodes, or it may become a chronic disease. There are many factors associated with the onset of pancreatitis, including direct injury, certain drugs, viral infections, heredity, hyperlipidemia (increased levels of blood fats), and congenital derangements of the ductal system. In Western society most cases are related either to alcoholism or to gallstones, especially when stones pass spontaneously into the ampulla of Vater. Although the immediate cause of acute pancreatitis is not always clear, it seems to involve one or more of the following factors: heavy stimulation of pancreatic acini; increased pressure within the duct because of partial obstruction (gallstones) or edema (alcohol); and damage to the fine ductal network in the gland, which allows the escape of activated, potent, and destructive digestive enzymes into the substance of the pancreas itself and into surrounding tissues. Overstimulation of mechanisms of secretory enzyme production in the acinar cell may also lead to the energizing of intracellular (lysosomal) enzyme systems, resulting in the conversion of proenzymes to active forms that begin to digest cellular organelles. The gland thus begins to self-destruct. Similar damage may appear in other body organs, such as the lungs, kidneys, and blood vessels, which receive these activated enzymes by way of the bloodstream. It is not clear how the proenzyme trypsinogen is converted to trypsin in the damaged acinar cell, but it is known that the activation of the other proenzymes proceeds from this conversion. The extent of acinar destruction appears to depend on the strength of the causative factors. Localized, severe abdominal and midback pain resulting from enzyme leakage, tissue damage, and nerve irritation is the most common symptom of acute pancreatitis. In severe cases, respiratory failure, shock, and even death may occur. The severity of the symptoms generally depends on the extent of the damage to the pancreas; the mortality rate approaches 50 percent in severe (hemorrhagic) pancreatitis but is less than 5 percent in milder forms. The diagnosis is confirmed by the detection of elevated levels of pancreatic enzymes (amylase and lipase) in the blood and, if islet cell function is disturbed by the inflammatory process, elevated blood glucose values. Ultrasonographic or computed tomographic scans of the upper abdomen usually reveal an enlarged and swollen pancreas. Sustained pain, often with fever, suggests the presence of a pseudocyst or abscess caused by localized areas of destruction and infections in the pancreas. Acute pancreatitis is treated primarily by supportive therapy, with replacement of fluid and salt and control of pain. In severe cases, washing necrotic material and active enzymes from the abdominal cavity during surgery may be beneficial. Following recovery from an acute attack, the prevention of further attacks should be the primary goal. Thus, the removal of gallstones, cessation of alcohol ingestion, lowering of blood fats through diet, and discontinuation of toxic drugs (glucocorticoids and thiazide diuretics, for example) can be helpful measures. In instances where repeated attacks of acute pancreatitis have resulted in strictures (scars) of the main pancreatic duct, surgical repair may prevent further attacks. Chronic pancreatitis Chronic pancreatitis rarely follows repeated acute attacks. It seems instead to be a separate disorder that results in mucus plugs and precipitation of calcium salts in the smaller pancreatic ducts. The progressive loss of acinar and islet cell function follows, presumably as a consequence of continuous inflammation resulting from the ductal blockage. Progressive calcification, which at times results in the formation of large stones in the major pancreatic ducts, has been attributed to diminished production of an acinar protein that normally holds calcium in solution. Alcoholism and certain hereditary factors account for almost all of the cases of chronic pancreatitis seen in Western countries. Chronic protein malnutrition is an important element in underdeveloped countries. Recurrent abdominal pain, diabetes, and intestinal malabsorption of dietary nutrients are the main symptoms of chronic pancreatitis. Weight loss and deficiencies of fat-soluble vitamins (A, D, E, and K) are common. Treatment includes abstinence from alcohol, management of diabetes with insulin, and ingestion of pancreatic enzyme supplements to control dietary malabsorption. Small intestine A lack of coordination of the inner circular and outer longitudinal muscular layers of the intestinal wall usually results in an accumulation of excess contents in the lumen, with consequent distension. This distension may cause pain and usually results in hyperactive contractions of the normal segment next to the distended area. Such contractions may be strenuous enough to produce severe, cramping pain. The most common cause of disturbed motility in the small intestine is food that contains an unsuitable additive, organism, or component. Traveler's diarrhea Traveler's diarrhea is watery, accompanied by cramps, and lasts a few days. It is almost always caused by toxin-generating Escherichia coli, less often by other organisms. Shigella infection may occur simultaneously, however, and visitors to countries where giardiasis is endemic may suffer infection. Salads remain the most common cause of traveler's diarrhea in countries where the climate is hot. Such diarrhea generally disappears spontaneously with abstention from food accompanied by drinking of nonalcoholic fluids. Mixtures of sodium and potassium chloride, sodium bicarbonate, and glucose reconstituted with water are one method of treatment. Stomach Indigestion The stomach moves in a rolling and wringing pattern, beginning about one-third of the way down the length of the organ, propelling the mixture of food and juices toward its outlet, the pylorus. Any disorder that affects the power of coordination of the stomach muscles is capable of producing symptoms ranging from those that are mildly unpleasant to others that are life-threatening. The unpleasant sensations, called anorexia and nausea, seem to be mediated through the central nervous system, with reflex input from nerve endings in the stomach and duodenum. Sometimes the entire duration of a nausea-vomiting episode is so short that it appears to be vomiting alone, obscuring the presence of nausea. This is characteristically noted in persons with primary diseases of the brain, especially those with tumours or meningitis in which the cerebrospinal fluid is under increased pressure. In many diseases, vomiting may not be preceded by nausea at all, and in others there may be a long time lag between nausea and vomiting. Seasickness is the best known example of this relationship. The intrinsic muscles of the stomach are innervated by branches of the vagus nerves, which travel along the esophagus from their point of emergence in the brain stem. Severing these nerves, as is often done in the surgical treatment of peptic ulcer, may produce temporary or more prolonged change in the ability of the stomach to empty itself. Many drugs, particularly the anticholinergic medications, are often used in the treatment of peptic ulcer. These drugs exert an action comparable to that produced by cutting the vagus nerves, but they have the potential disadvantage of reducing the flow of saliva, interfering with vision by disturbing accommodation reflexes in the pupil, and reducing the power of the muscle on which bladder emptying depends. Gastric retention may result from the degeneration of the nerves to the stomach that can result from diabetes mellitus. Obstruction due to scarring in the area of the gastric outlet, or to tumours encroaching on the lumen, causes the stomach to fill up with its own secretions as well as with partially digested food. In these circumstances, vomiting leads to dehydration and to electrolyte losses, which threaten life if not corrected. The ingestion of soluble alkali in this situation may aggravate the disturbance in the acidbase balance of the body. Bulimia, a nervous disorder characterized by compulsive eating followed by vomiting and purging, can cause severe dehydration and even a ruptured stomach, and it can prove fatal. Ulcerative diseases The area of the stomach in which acid and pepsin are secreted has the highest resistance to peptic ulcer. The mucosa elsewhere is less well protected, and its breakdown may lead to ulceration. If the breach is confined to the superficial layers of the mucosa, it is called an erosion; if it extends through the intrinsic layer of muscle of the mucosa into the tissues below, it is known as an ulcer. Erosions and ulcers can be acute or chronic according to how readily they heal. The circumstances that contribute to mucosal injury and ulcer formation include physical and chemical trauma that result from hot fluids and food, aspirin and other drugs, irritating spices, and pickling fluids. Reduction of the secretion of mucus by the stomach and duodenum, or a reduction of bicarbonate secretion (which neutralizes excess acid), lowers resistance. Extracellular paracrine messenger substances, in particular the prostaglandins, which stimulate secretion of mucus and bicarbonate and also stimulate cell replication, may be deficient in the mucosa of individuals with peptic ulcer. The rate of cell replication is lowered by malnutrition. In the United States and the Western world generally, duodenal ulcer is much more common than gastric ulcer, occurs more often in men than in women, and is aggravated by nervous tension and fatigue. In Japan, gastric ulcer is more common than duodenal ulcer and is thought to be related to the raw fish and acetic acid pickles of the traditional diet. In 60 percent of persons with duodenal ulcer, acid and pepsin secretion is on the high end of normal, and in 40 percent, it is above normal. Of particular concern in duodenal ulcer is the inappropriate secretion of acid and pepsin due to failure of homeostatic-controlling mechanisms, so that it continues when the stomach is empty and during the night hours. In special circumstances such as the state of shock produced by large burns, intracranial surgery, coronary occlusion, and septicemia, acute and rapidly penetrating ulcers may occur. Genetic factors are involved in the development of ulcers. Inheriting blood group O and an inability to secrete antigen substance H into body fluids, while secreting the Lewis antigen, renders a person four times more likely to develop duodenal ulceration than average. There are families in whom the secretion of pepsinogen I is excessive and renders them prone to duodenal ulcer since excess acid secretion is linked to excess pepsinogen I secretion. Possession of blood group A increases the chance of developing a gastric ulcer. Otherwise, the secretion of acid and pepsin in individuals with gastric ulcer is normal in all respects. There are other distinct differences between ulcers at the two main sites: duodenal ulcer is most common between 25 and 35 years of age, while gastric ulcer is uncommon before 40 years and has a peak frequency between 55 and 65 years. Pain is the major symptom of duodenal ulcers. The pain is a burning or gnawing sensation felt in the upper abdomen in the midline below the sternum. In gastric ulcer it comes on soon after eating, whereas in duodenal ulcer it comes on when the stomach is empty, one and a half to two hours after meals and during the night hours. In the early stages of the disease, the pain is easily and immediately relieved by alkalis and, in duodenal ulcer, by light food. Peptic ulcers naturally show remissions and relapse. Attacks last from four to eight weeks before spontaneously ceasing. In most instances this behaviour corresponds to healing and breakdown of the ulcer, but an active ulcer may produce no symptoms. Gastric ulcers are slower than are duodenal ulcers to pass into remission and to respond to treatment. The fluctuating course of activity continues for five to 20 years or more. At some point in this span, the symptoms disappear in 60 percent of the individuals, never to recur. Of the remainder, 20 percent have surgery at some time because of complications and resistance to cure, and 20 percent have some degree of disability throughout their lives. Gastric ulcers almost always recur in the same site within the stomach, but duodenal ulcers are often multiple and recurrence may be anywhere in the bulb. Furthermore, duodenal ulcers are usually accompanied by an inflammation affecting the whole of the bulb (duodenitis). Multiple erosions varying in size between 0.5 and five millimetres are frequently scattered over the mucosa. With gastric ulcers the inflammation is usually confined to the immediate vicinity of the crater and, as a rule, is not accompanied by erosions. The exceptions are gastric ulcers in the antrum and prepyloric area associated with the use and abuse of analgesics and nonsteroidal anti-inflammatory drugs for arthritic disorders, in which multiple erosions are commonly present. The most common site of gastric ulcers is halfway up the inne

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