digestive system disease

digestive system disease


      any of the diseases that affect the human digestive tract. Such disorders may affect the esophagus, stomach, small intestine, large intestine (colon), pancreas, liver, or biliary tract. A prevalent disorder of the digestive system is gastroesophageal reflux disease (i.e., the passage of gastric contents into the esophagus), which causes heartburn on a regular basis in some individuals. cirrhosis of the liver primarily results from excessive alcohol consumption, but it may also develop after infection with the hepatitis C virus. Other common diseases of the digestive system include peptic ulcers (peptic ulcer), colorectal cancer, and gallstones (gallstone). Many disorders of the digestive system can be prevented by a diet low in fats and high in fruits and vegetables, limited alcohol consumption, and periodic medical examinations.

      This article discusses the common infections, inflammations, ulcers, and cancers that affect each organ of the digestive tract. For a detailed discussion of the anatomy and physiology of the digestive system, see digestive system, human.

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. Multiple brown freckles on the lips associated with polyps (polyp) in the small intestine is characteristic of Peutz-Jeghers syndrome. Aggregates of small yellow spots on the buccal mucosa and the mucosa behind the lips due to the presence of enlarged sebaceous glands just below the mucosal surface indicate Fordyce disease.

      The most common mouth ulcers (ulcer) are due to aphthous stomatitis (canker sore). These ulcers affect one out of every five Caucasians. The manifestations of this condition range 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 (about half an inch) or more in diameter. The ulcers are frequently multiple, occur anywhere in the mouth, and may persist for months at a time. Symptoms range 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 stress, but it may also be a reflection of an underlying malabsorptive disease such as celiac disease. Treatment is directed to the predisposing cause. Topical and systemic corticosteroids are the most effective treatment. Local anesthetic agents and analgesics (analgesic) may permit easier talking and eating. In a more serious condition, Behçet syndrome, similar ulcers occur in the mouth and on the genitalia, and the eyes may become inflamed.

      Discoloration of the tongue, commonly white, is due to deposits of epithelial debris, effete (or worn-out) bacteria, and food. It also occurs in circumstances in which there is reduced saliva production. This may be acute, as in fever, when water loss through the skin is excessive. Discoloration of the tongue becomes chronic following atrophy of the salivary 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 furlike filiform papillae (black hairy tongue) may be due to a fungus with pigmented filaments. Occasionally it simply represents excessive elongation of the filiform papillae.

      A bald tongue (atrophic glossitis), with a smooth surface due to complete atrophy of the papillae, is associated with malnutrition, severe iron deficiency anemia, pernicious anemia, and pellagra, a disorder of skin and mucous membranes due to niacin deficiency. 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 caused by syphilis, scarlet fever, or typhoid fever. 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 areas gradually become re-epithelialized with regrowth of the filiform papillae, only for the inflammatory process to begin elsewhere in the tongue. Thus, 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. There is no treatment.

      Vincent disease (Vincent gingivitis) (trench mouth) is an ulcerating, necrotizing infection of the gingiva (gums) characterized by spontaneous bleeding from affected areas and 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 it is transmitted by the exchange of saliva in kissing, but its epidemic increase in wartime and its frequency in the sexually promiscuous suggest this. Vincent disease is treated with antibiotics (antibiotic) followed by trimming of the gum margins to eliminate subgingival pockets.

       oral cancer is sometimes caused by chronic thermal irritation in heavy smokers and is often preceded by leukoplakia (plaquelike patches arising on the mucous membranes of the cheeks, gum, or tongue). Similarly, oral cancer can be caused by the habit of keeping tobacco 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 (lymphoma) 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, or cavities, 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. 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. 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 (foul breath) is due to the rotting debris in the pockets under the gum margins. Eventually the teeth loosen and fall out or need to be extracted. The resistance of the dental enamel to damage by organic acids is increased by fluoride, and in many countries this is incorporated into toothpaste formulas 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.

      Inflammation of the posterior wall of the mouth and of the tonsils and adjoining tissue on each side of the oral pharynx is very common, especially in young persons. Such infections are due to bacteria of the streptococcal and staphylococcal species or from viral infections. In viral pharyngitis the tissue is usually less red and swollen than is true of streptococcal pharyngitis, and it is less often covered by a whitish exudate (protein-rich fluid). Other tonsillar tissue in the upper part of the pharynx and at the root of the tongue may be similarly involved. In diphtheritic pharyngitis, the membranous exudate is more diffuse than in other types of pharyngitis, it is tougher, and it extends over a much larger part of the mucous membrane of the mouth and nose. One of the complications of tonsillitis or pharyngitis may be a peritonsillar abscess, also called quinsy, adjacent to one tonsil; this appears as an extremely painful bulging of the mucosa in the area. Surgical incision and draining are sometimes necessary if antibiotics are not given promptly.

Congenital defects
       cleft lip, also known as harelip, is a congenital (congenital disorder) deformity in which the central to medial lip fails to fuse properly, resulting in a fissure in the lip beneath the nostrils. Other disorders are related to an abnormal position of the teeth and the jaws, resulting in inefficient chewing, and to the absence of one or more of the salivary glands, which may lessen the amount and quality of saliva that they produce. Neurological defects that provide inadequate stimulation to the muscles of the tongue and the pharynx can seriously impair chewing and even swallowing. Sensory-innervation defects may not allow the usual reflexes to mesh smoothly, or they may permit harmful ingestants to pass by undetected.

Salivary glands
      The secretion of saliva is markedly diminished in states of anxiety and depression. The consequent dry mouth interferes with speech, which becomes thick and indistinct. In the absence of the cleansing action of saliva, food debris persists in the mouth and stagnates, especially around the base of the teeth. The debris is colonized by bacteria and causes foul breath (halitosis). In the absence of saliva, swallowing is impeded by the lack of lubrication for the chewing of food that is necessary to form a bolus. The condition is aggravated in states of anxiety and depression when drugs that have an anticholinergic-like activity (such as amitriptyline) are prescribed, because they further depress the production of saliva. The salivary glands (salivary gland) are severely damaged and atrophy in a number of autoimmune disorders such as Sjögren disease (Sjögren's syndrome) and systemic lupus erythematosus (lupus erythematosus). The damage occurs partly by the formation of immune complexes (antigen-antibody associations), which are precipitated in the gland and initiate the destruction. In these circumstances, the loss of saliva is permanent. Some symptomatic relief is obtained by the use of “artificial saliva,” methylcellulose mouthwashes containing herbal oils such as peppermint. As some of the salivary glands retain their function, they may be stimulated by chewing gum and by a parasympathomimetic agent such as bethanecol. The production of saliva may be also impaired by infiltration of the salivary glands by pathological lymphocytes, such as in leukemias (leukemia) and lymphomas (lymphoma). In the early stages of these diseases, the glands swell and become painful.

      Excessive production of saliva may be apparent in conditions interfering with swallowing, as in Parkinson disease (parkinsonism), or in pseudobulbar paralysis from blockage of small arteries to the midbrain regions. True salivary hypersecretion is seen in poisoning due to lead or mercury used in certain industrial processes and as a secondary response to painful conditions in the mouth, such as aphthous stomatitis (certain ulcers of the oral mucosa) and advanced dental caries.

      Acute and painful swelling of salivary glands develops when salivary secretion is stimulated by the sight, smell, and taste of food but saliva is prohibited from flowing through an obstructed salivary duct. Swelling and pain subside between meals. Diagnosis can be confirmed by X ray. Persistent swellings may be due to infiltration by benign or malignant tumours or to infiltration by abnormal white blood cells, as in leukemia. The most common cause of acute salivary swelling is mumps.

      Difficulty in swallowing (dysphagia) may be the only symptom of a disorder of the esophagus. Sometimes dysphagia is accompanied by pain (odynophagia), or pain may occur spontaneously without swallowing being involved. The esophagus does nothing to alter the physical or chemical composition of the material it receives, and it is poorly equipped to reject materials that have got past the intricate sensors of the mouth and throat. Consequently, it is vulnerable to mucosal injury from ingestants as well as to materials that reflux into its lower segment from the stomach. Although the esophageal muscle coats are thick, the esophagus is not protected with a covering of serous membrane, as are neighbouring organs in the chest.

Congenital defects
      Congenital (congenital disorder) defects of the esophagus are most often seen in infancy, primarily as a failure to develop normal passageways. Infants born with openings between the esophagus and trachea cannot survive without early surgery. The lower end of the esophagus is subject to various developmental abnormalities that shorten the organ so that the stomach is pulled up into the thoracic cavity. Abnormalities of the diaphragm may contribute to a similiar outcome.

Inflammatory disorders
      Inflammatory (inflammation) disorders of the esophagus result from a variety of causes, from the ingestion of noxious materials, the lodgment of foreign bodies, to a complex of events associated with reflux of gastric contents from the stomach into the lower esophagus. Inflammation resulting from surface injury by caustic substances is called corrosive esophagitis. When the problem is associated with reflux, the term peptic esophagitis is applied to inflammation involving both the mucous membrane and the submucosal layer. A number of other diseases may cause inflammation of the esophagus, e.g., scleroderma, a disease in which the smooth muscle of the organ degenerates and is eventually replaced by fibrous tissue, and generalized candidiasis, a disease in which the esophagus is often involved in a septic process characterized by many small abscesses and ulcerations.

      Fibrous ( scar) tissue contracts over time. Consequently, when fibrous tissue develops around a tube, as in the esophagus, in response to inflammation, the contracting scar narrows the lumen, causing a stricture, and may eventually obstruct it completely. Strictures are readily diagnosed by X ray or esophagoscope.

       dysphagia is characterized by difficulty in swallowing caused by lesions, failure to transport a bolus through the esophagus, or mechanical obstruction by stricture, tumours, or foreign bodies in the esophagus. In persons over 50 years of age, the sensation of food “sticking” is more often caused by a disease process, frequently a tumour, involving the wall of the esophagus and providing a mechanical rather than a functional obstacle to the passage of food. The neural arc of swallowing involves the medulla (medulla oblongata) of the brain stem, the vagus (10th cranial) nerves, and the glossopharyngeal, trigeminal, and facial nerves. Consequently, dysphagia may also result from interference with the function of any part of this pathway. Thus, it occurs commonly, but usually transiently, in strokes (stroke). Dysphagia may be prominent in degenerative diseases of the central nervous system, especially of the ganglia at the base of the brain. In these circumstances, the behaviour of the smooth muscle of the pharynx and the upper esophageal sphincter is disturbed.

      Most individuals can locate the site of dysphagia and the distribution of the pain with accuracy. A sense of food sticking or of pain on swallowing, however, may be felt to be in the throat or upper sternum when the obstruction or disease is in fact at the lower end of the esophagus. The sensation of a “lump in the throat,” or “globus hystericus,” is not connected with eating or swallowing. The sensation may result from gastroesophageal reflux or from drying of the throat associated with anxiety or grief. Treatment is directed toward the cause of the disorder.

      The nerves conveying the sense of pain from the esophagus pass through the sympathetic system in the same spinal cord segments as those that convey pain sensations from the muscle and tissue coverings of the heart. As a result, episodes of pain arising from the esophagus as a result of muscle spasm or transient obstruction by a medicine tablet or other object may be experienced in the chest and posterior thorax and radiate to the arms. This pain thus mimics pain of cardiac origin (angina). The pain due to transient obstruction may be felt not only in the chest but also, through radiation to the back, between the shoulder blades. It is very similar to pain from gallstones (gallstone); attacks last 10 to 30 minutes.

      In middle-aged and elderly persons, spontaneous and diffuse spasm of the smooth muscle of the esophagus causes considerable discomfort as well as episodes of dysphagia. Alternative names for the condition are “corkscrew” esophagus and diffuse spasm of the esophagus. The appearance of the esophagus seen on an X-ray screen while a barium bolus is swallowed resembles that of the outline of a corkscrew because of the multiple synchronized contractions at different levels of the spirally arranged smooth muscle. The pain of esophageal spasm may be relieved by medications that relieve cardiac angina, especially nitroglycerin or nifedipine.

      Disorders of the motility of the esophagus tend to be either caused by or aggravated during times of stress. Eating rapidly is another trigger, as this demands more precise and rapid changes in muscle activity than eating slowly. Achalasia, formerly called cardiospasm, is a primary disturbance in the peristaltic action of the esophagus that results in failure to empty the organ of its contents. The lower sphincteric portion of the esophagus does not receive its normal signal to relax and, over time, may become hypertonic, resisting stretching. A cycle occurs in which the main portion of the esophagus slowly becomes distended, holding a column of fluid and food that it cannot propel downward to a lower esophageal sphincter that stays closed because of a failure in its neural system. In most persons with this disorder, there is a shortage or disease of ganglion cells of the myenteric plexus (Auerbach plexus), or a disease of the network of nerves within the muscles of the esophagus, so that coordinated peristalsis becomes impossible. In Chagas disease (Chagas' disease), parasites called trypanosomes invade the neural tissue and directly destroy ganglion cells. These organisms are not present in the temperate zones of the world, however, and the reason for ganglion cell degeneration in achalasia is generally unknown. Effective treatment is achieved by destroying the ability of the lower esophageal sphincter of the esophagus to contract. This may be done by forcible dilatation, using a balloon, of the esophagus in the area that is tonically contracted. The objective is to rupture the circular muscle at the site, and this is generally achieved with one or two dilatations. If this fails to overcome the contraction or if the contraction recurs, surgery is required that involves opening the abdomen and cutting through the circular muscles from the outside of the esophagus. The disadvantage of both methods of treatment is that the anti-reflux mechanism is thereby destroyed. Consequently, if precautions are not taken, the individual may lose the symptoms and risks of achalasia but may develop the symptoms and signs of reflux peptic esophagitis.

Gastroesophageal reflux (gastroesophageal reflux disease)
      In healthy individuals, reflux of gastric contents into the esophagus occurs occasionally. This causes the burning sensation behind the sternum that is known as heartburn. Some of the refluxed material may reach the pharynx where it also may be felt as a burning sensation. Reflux is most likely to occur after large meals, especially if physical activity, including bending, stooping, or lifting, is involved. In these circumstances, the esophagus responds with peristaltic waves that sweep the gastric contents back into the stomach, with relief of the heartburn.

      Persistent reflux symptoms are invariably due to inadequate functioning of the anatomical components, such as the lower esophageal sphincter, which keep the contents of the stomach below the diaphragm, delayed esophageal clearance of the refluxed material, and delayed emptying of the stomach. The disorder can also be caused by obesity. Excessive fat on the trunk is almost always accompanied by large deposits of fat within the abdomen, especially in the mesentery (the curtainlike structure on which most of the intestine is hung). Consequently, when intra-abdominal pressure is increased, such as in physical activity, there is insufficient room within the abdomen to accommodate the displacement of the organs, and the resulting pressure forces the stomach upward. The weak point is the centre of the diaphragm at the opening (hiatus) through which the esophagus passes to join the stomach. The upper portion of the stomach is pushed through the hiatus, and the distortion of the position of the organs brings about impaired functioning of the anti-reflux mechanisms. In the early stages the stomach may slide back into the abdomen when the increase in the intra-abdominal pressure eases, but eventually, if the circumstances are unchanged, the upper part remains above the diaphragm. A common contributory cause of gastroesophageal reflux in women is pregnancy. As the uterus containing the developing fetus comes to occupy a large part of the abdomen, the effect is the same as in obesity. Because gravity is the only force that keeps the gastric contents within the stomach, if a hernia develops, the reflux and the symptoms from it will promptly occur when the individual lies down. Persisting reflux of gastric contents with acid and digesting enzymes leads to chemical inflammation of the lining of the esophagus and ultimately to peptic ulceration. If inadequately treated, the process leads to submucosal fibrosis and stricturing, and, besides the symptoms of heartburn and regurgitation, the patient experiences pain on eating and swallowing.

      The treatment of peptic reflux esophagitis includes losing weight, avoiding acidic and fatty foods and beverages, remaining upright for two to three hours after meals, giving up smoking, and raising the head of the bed high enough to discourage nocturnal gastroesophageal reflux. Antacids are effective, as are medications that reduce the secretion of acid by the stomach, such as histamine receptor antagonists and proton pump inhibitors. If a stricture has formed, it can be dilated easily. If the disorder is not overcome with these conservative measures, surgical repair is performed through either the chest or the abdomen.

      Some individuals with severe peptic reflux esophagitis develop Barrett esophagus, a condition in which the damaged lining of the esophagus is relined with columnar cells. These cells are similar to those lining the upper part of the stomach and are not the usual squamous cells that line the esophageal mucosa. In some persons in whom this transformation occurs, a carcinoma develops some 10 to 20 years later. The decision as to the treatment of a hiatal hernia by conservative means or by surgery is influenced by such factors as age, occupation, and the likelihood of compliance with a strict regimen.

      There is a much less common form of hiatal hernia, called a paraesophageal hernia, in which the greater curvature of the stomach is pushed up into the thorax while the esophagogastric junction remains intact below the diaphragm. Such individuals experience dysphagia caused by compression of the lower esophagus by the part of the stomach that has rolled up against it. This rarer form of hernia is more dangerous, often being complicated by hemorrhage or ulceration, and requires relief by surgery.

Diverticula (diverticulum)
      Pouches in the walls of the structures in the digestive system that occur wherever weak spots exist between adjacent muscle layers are called diverticula. In the upper esophagus, diverticula may occur in the area where the striated constrictor muscles of the pharynx merge with the smooth muscle of the esophagus just below the larynx. Some males over 50 years of age show protrusion of a small sac of pharyngeal mucous membrane through the space between these muscles. As aging continues, or if there is motor disturbance in the area, this sac may become distended and may fill with food or saliva. It usually projects to the left of the midline, and its presence may become known by the bubbling and crunching sounds produced during eating. Often the patient can feel it in the left side of the neck as a lump, which can be reduced by pressure of the finger. Sometimes the sac may get so large that it compresses the esophagus adjacent to it, producing a true obstruction. Treatment is by surgery. Small diverticula just above the diaphragm sometimes are found after the introduction of surgical instruments into the esophagus.

      Boerhaave syndrome is a rare spontaneous rupture to the esophagus. It can occur in patients who have been vomiting or retching and in debilitated elderly persons with chronic lung disease. Emergency surgical repair of the perforation is required. A rupture of this type confined to the mucosa only at the junction of the linings of the esophagus and stomach is called a Mallory-Weiss lesion. At this site, the mucosa is firmly tethered to the underlying structures and, when repeated retching occurs, this part of the lining is unable to slide and suffers a tear. The tear leads to immediate pain beneath the lower end of the sternum and bleeding that is often severe enough to require a transfusion. The circumstances preceding the event are commonly the consumption of a large quantity of alcohol (alcoholism) followed by eating and then vomiting. The largest group of individuals affected are alcoholic men. Diagnosis is determined with an endoscope. Most tears spontaneously stop bleeding and heal over the course of some days without treatment. If transfusion does not correct blood loss, surgical suture of the tear may be necessary. An alternative to surgery is the use of the drug vasopressin, which shuts down the blood vessels that supply the mucosa in the region of the tear.

      Esophageal tumours may be benign or malignant. Generally, benign tumours originate in the submucosal tissues and principally are leiomyomas (tumours composed of smooth muscle tissue) or lipomas (tumours composed of adipose, or fat, tissues). Malignant tumours are either epidermal cancers, made up of unorganized aggregates of cells, or adenocarcinomas, in which there are glandlike formations. Cancers arising from squamous tissues are found at all levels of the esophagus, whereas adenocarcinomas are more common at the lower end where a number of glands of gastric origin are normally present. Tumours produce difficulty in swallowing, particularly of solid foods; they are much more common in men than in women, and they seem to vary greatly in their worldwide distribution. In North China, for example, the incidence of esophageal cancer in men is 30 times that of white men in the United States and 8 times that of black men. The exact causes of esophageal cancer are not known. Risk factors may include age, sex, smoking, excessive consumption of alcohol, Barrett esophagus, and a personal history of cancer.

      In women, cancer of the upper esophagus is more common than in men, and women may be predisposed by long-standing iron deficiency, or Plummer-Vinson (Paterson-Kelly) syndrome. Dysphagia is the first and most prominent symptom. Later swallowing becomes painful as surrounding structures are involved. Hoarseness indicates that the nerve to the larynx is affected. The diagnosis is suggested by X ray and proved by endoscopy with multiple biopsies from the area of abnormality. Diagnosis can be reinforced by removing quantities of cells with a nylon brush for examination under a microscope (exfoliative cytology). The prognosis is poor because the tumour has usually been growing for one or two years before symptoms are apparent. The channel of the esophagus is encroached upon and can be almost entirely obstructed. Esophageal cancer is usually accompanied by considerable weight loss, but nutrition may be restored by nutritional supplements. In advanced cases, a tube may be inserted into the esophagus to keep it open. Where the channel is greatly narrowed, the size of the tumour can be reduced by destroying the tissue with lasers. Radiotherapy is used for malignancies of the upper esophagus and as treatment for those at the lower end. A combination of radiotherapy followed by surgical excision may also be used. The five-year survival rate for esophageal cancer remains very low. Lessening the effects of the disease, with restoration of eating ability, is very important, because otherwise the inability to swallow even saliva is distressing and starvation may result.

      Indigestion, also called dyspepsia, is any or all of the unpleasant symptoms that are associated with the malfunctioning of the digestive system. Indigestion may be caused by a disease, but it primarily occurs because of stress or improper eating habits, smoking, drinking excessive quantities of coffee or alcohol, or hypersensitivity to particular foods. Any disorder that affects the coordination of the stomach muscles is capable of producing symptoms ranging from those that are mildly unpleasant to others that are life-threatening. Symptoms include abdominal discomfort, belching, flatulence, anorexia, nausea, vomiting, diarrhea, constipation, and heartburn. 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 (brain cancer) 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 the two. Seasickness is the best-known example of this relationship.

      The intrinsic muscles of the stomach are innervated by branches of the vagus nerves (vagus nerve), which travel along the esophagus from their point of emergence in the brain stem. Gastric retention may result from the degeneration of these nerves that can result from diabetes mellitus. Obstruction due to scarring in the area of the gastric outlet, or to tumours (stomach cancer) 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 acid-base balance of the body. Bulimia (bulimia nervosa), 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 (ulcer) diseases
 Ulcers are produced when external factors reduce the ability of the mucosal lining to resist the acidic effects of gastric juice (a mixture of digestive enzymes and hydrochloric acid). 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 lesion 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. Infection with the bacterium Helicobacter pylori and long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) are the two major causes of ulcers. 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.

      In the Western world duodenal ulcer is much more common than gastric ulcer, occurs more often in men than in women, and is aggravated by stress. 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. 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. Genetic (genetic disease, human) factors are also involved in the development of ulcers. Inheriting blood group O may render a person more likely to develop duodenal ulceration. 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 secretion of this hormone.

      Pain is the major symptom of duodenal ulcers. The pain is a burning or gnawing sensation felt in the midupper abdomen. 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 antacids and, in duodenal ulcer, by light food.

      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 duodenal bulb. Furthermore, duodenal ulcers are usually accompanied by an inflammation affecting the whole bulb (duodenitis). Multiple erosions varying in size between 0.5 and 5 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 NSAIDs for arthritic disorders, in which multiple erosions are commonly present.

      The most common site of gastric ulcers is halfway up the inner curvature of the stomach at the junction of the lower one-third with the upper two-thirds of the organ. This may be because blood flow to this site is more easily reduced than elsewhere. Chronic gastric ulcers at this site are strongly associated with obstructive disease of the airways (chronic bronchitis and emphysema). Smoking impairs the healing of both gastric and duodenal ulcers.

      Infection with H. pylori is the most common bacterial infection in humans; it is pervasive in the Third World, and in the United States it affects about a third of the population. Among those who suffer from peptic ulcers, as many as 90 percent of those with duodenal ulcers and 70 percent with gastric ulcers are believed to be infected with H. pylori. This bacterium converts the abundant waste product urea into carbon dioxide and ammonia. The process causes the mucosal lining to break down. In its weakened condition the lining cannot withstand the corrosive effects of gastric acid, and an ulcer can form.

      The complications of peptic ulcers are hemorrhage, perforation, and obstruction of the outlet of the stomach (pyloric stenosis) by scarring of the duodenal bulb or of the pyloric channel. Scarring often leads to bouts of vomiting and accompanying malnutrition and requires surgery. Bleeding (bleeding and blood clotting) may be obscured because of oozing from the floor of the ulcer and detectable only by laboratory testing of the feces, or bleeding may be brisk, leading to the passage of tar-coloured stools (melena). Occasionally, when the ulcer erodes into a large vessel, bleeding is excessive and life-threatening. The mortality associated with bleeding is high in the elderly because of chronic changes in the lungs, heart, and blood vessels, which reduces cardiorespiratory reserves. This is further aggravated by smoking. Brisk bleeding is usually accompanied by the vomiting of blood (hematemesis), which requires treatment by blood transfusion. In the elderly, hardening of the arteries ( atherosclerosis) prevents the vessel from closing down around the lesion. If bleeding persists or recurs, surgery is necessary. Ulcers that penetrate the back wall of the stomach or duodenum erode into the pancreas, and back pain becomes prominent. If the ulcer penetrates the anterior wall, free perforation into the abdominal cavity may occur. This causes immediate, intense pain and shock, and the abdominal wall becomes rigid. In most instances this requires emergency surgery with drainage of the abdomen.

      Surgery for chronic ulceration is used less frequently since the introduction of drugs that stop the secretion of stomach acid. Histamine-receptor antagonists, such as cimetidine, ranitidine, and famotidine, block the action of histamine on the acid-secreting parietal cells of the stomach. Proton pump inhibitors, such as omeprazole, lansoprazole, and rabeprozale, inhibit the ATPase enzyme inside the parietal cell and prevent acid secretion. Most peptic ulcers not caused by H. pylori infection result from the ingestion of large quantities of NSAIDs. Withdrawal of NSAID treatment usually allows the ulcer to heal. Treatment for H. pylori–induced ulcers are antibiotics and a proton pump inhibitor.

      A diffuse inflammation of the stomach lining, gastritis is usually an acute disorder caused by contaminated food, by alcohol abuse, or by bacterial- or viral-induced inflammation of the gastrointestinal tract ( gastroenteritis). Such episodes are short-lived and require no specific treatment. Pain is generalized in the upper abdomen and is continuous, but it progressively subsides over two or three days. Aspirin and NSAIDs taken for arthritis cause erosions in the antrum of the stomach and in some instances cause bleeding and chronic ulceration. Infection by the bacteria H. pylori is also a common cause of chronic gastritis. This usually responds to the withdrawal of the offending drugs and treatment with the same agents used to treat peptic ulcers of the stomach and duodenum.

      Another form of gastritis is gastric atrophy, in which the thickness of the mucosa is diminished. Gastric atrophy is often the culmination of damage to the stomach over many years. Diffuse gastric atrophy leads to partial loss of the glandular and secreting cells throughout the stomach and may be associated with iron deficiency anemia. Atrophy of the mucosa confined to the body and fundic regions of the stomach is seen in pernicious anemia and is due to the formation of antibodies to intrinsic factor secreted by the parietal cells. Intrinsic factor is necessary to the absorption of 12 (vitamin B12).

      Malignant tumours (stomach cancer) of the stomach are common, but the incidence of stomach cancer varies from country to country, probably a result of both genetic and environmental factors. stomach cancer often occurs in older persons whose stomachs produce only small quantities of acid. Infection with H. pylori–associated chronic gastritis may be a risk factor in developing stomach cancer. Stomach cancer affects men more often than women and accounts for about 10 percent of all deaths from cancers of the gastrointestinal tract in the United States. In Japan, on the other hand, it accounts for nearly 80 percent of such cancers in males, possibly due to diet.

      Other malignant tumours that involve the stomach are ordinarily made up of lymphoid and connective tissue. Benign tumours, especially leiomyomas, are common and may, when large, cause massive hemorrhage. Polyps of the stomach are not common except in the presence of gastric atrophy. Treatment for these tumours, benign or malignant, is surgery.

      Because symptoms produced by tumours of the stomach are highly variable, there are no common characteristics of the disease in its early stages. The symptoms most often seen are loss of appetite, some weight loss, and symptoms attributable to anemia, a condition that frequently is present because of blood loss into the stools, which, though constant, is usually so minimal as to escape notice by the patient. Tumours in the lower part of the stomach produce obstructive symptoms, and tumours high in the stomach may obstruct the esophageal entry into the stomach, producing difficulty in swallowing. Although pain is usually mild, it may be the most noticeable symptom. Stomach cancers often spread to neighbouring lymph nodes or to the liver.

      The duodenum is often involved in the diseases of its neighbours, in particular the pancreas and the biliary tract. Primary cancer of the duodenum is an infrequent disease. Benign tumours, particularly polyps and carcinoids, are more frequent. Cancers of the common bile duct or of the pancreas may make their presence known by obstruction of the duodenum and pain. These cancers often are diagnosed by upper intestinal X-ray studies, endoscopy, ultrasound, or computed tomography (CT) scanning. Benign anomalies of the organs of this area, like an encircling ring of pancreas, may also encroach upon the duodenum. In countries of the Middle and Far East, where parasites are endemic, roundworms and tapeworms in particular are often found anchored in the duodenum. In inflammations of the pancreas, the motility of the neighbouring duodenum is often impaired, and occasionally ulceration with hemorrhage occurs. A protozoal parasite, Giardia lamblia, can contaminate drinking water and is a common cause of diarrhea and, if unrecognized, malabsorption.

      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 intestinal 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 the abnormally swift passage of watery waste material through the large intestine, with consequent discharge of loose feces. Traveler's diarrhea is accompanied by cramping and lasts a few days. It is almost always caused by toxin-generating Escherichia coli. Shigella infection may occur simultaneously, however, and visitors to countries where giardiasis is endemic may suffer infection. Contaminated 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.

Intestinal obstruction
      The most serious problems in small intestine motor disturbances arise from an intestinal obstruction that results from encroachment on the bowel by an adhesive band or from internal blockage produced by a tumour or gallstone. Serious complications result when a portion of the intestine undergoes partial necrosis, or death, from lack of blood supply. The necrotic section cannot participate in peristaltic activity and, for all practical purposes, serves as an obstruction. The death of the tissue, furthermore, results in the escape of highly toxic fluids from the intestinal contents through the wall, producing peritonitis. The symptoms and treatment of intestinal obstruction depend on the nature of the obstruction and its location. Surgery is often necessary.

      The common disorder known as irritable bowel syndrome (IBS) is probably due to a disturbance of the motility of the whole intestinal tract or to increased sensitivity of the large intestine. The symptoms vary from watery diarrhea to constipation and the passage of stools with difficulty. When the colon is involved, an excess of mucus is often observed in the stools. Pain and cramping are most often felt in the lower abdomen. Generalized abdominal discomfort, sometimes with nausea, may follow defecation and may last 15 to 30 minutes. Many sufferers experience high levels of stress, and some have periods of anxiety depression.

      Occasionally irritable bowel syndrome may be due to an allergy to specific foods. IBS may develop following an infection such as bacillary dysentery, after which the small intestine remains irritable for many months. Treatment of IBS includes elimination of stress, psychological support, change in lifestyle, and exercise. Possible aggravating items such as lactose-containing foods, coffee, and deep-fried dishes should be eliminated from the diet, and dietary fibre should be added to help in resolving constipation. When discomfort is prominent, antispasmodic agents that relax smooth muscle, such as dicyclomine hydrochloride or mebeverine, may be prescribed. If diarrhea does not respond to dietary measures, diphenoxylate or loperamide may slow the movement of the intestinal contents, thereby increasing the potential for the reabsorption of water.

      Malabsorption occurs when the small intestine is unable to transport broken-down products of digestive materials from the lumen of the intestine into the lymphatics or mesenteric veins, where they are distributed to the rest of the body. Defects in transport occur either because the absorptive cells of the intestine lack certain enzymes, whether by congenital defect or by acquired disease, or because the cells are hindered in their work by other disease processes that infiltrate the tissues, disturb motility, permit bacteria to overpopulate the bowel, or block the pathways over which transport normally proceeds. Malabsorption also may result from pancreatitis, cystic fibrosis, obstruction of the bile ducts or lymphatic vessels, or surgical removal of a section of the small intestine.

      Diagnosis of malabsorption is determined primarily from the patient's history, physical examination, X-ray films of the abdomen, and study of the stools under controlled dietary conditions. Motor aspects of the intestine can be studied using a variety of techniques. A biopsy of the small intestine may also be performed to detect abnormalities.

Congenital malformations
      Meckel diverticulum is a common congenital malformation that occurs when the duct leading from the navel to the small intestine in the fetus fails to atrophy and close. The duct serves as the principal channel for nourishment from the mother. The diverticulum in the child or adult may range from a small opening to a tube that is a foot or more in length; it may contain cells derived from the stomach glands that secrete acid and pepsin. If such secretions spill onto intestinal mucosa, the mucosa ulcerates and often bleeds. Thus a peptic ulcer can develop at a site far from the stomach or duodenum. The peptic ulcer gives rise to pain, bleeding, or obstruction, and it is the most common cause of bleeding from the lower intestine in children. Meckel diverticulum must be treated surgically if complications develop.

      Another congenital problem in the small intestine is the presence of multiple diverticula (diverticulum), or outpouchings of mucosa and serosa. Multiple diverticula are seen usually in elderly persons, although occasionally one may be the site of acute inflammation in a young adult. bacteria flourish in these diverticula because the outpouchings have no motor activity and cannot empty themselves. The bacteria deprive the body of nutrients and may cause diarrhea and serious malabsorption. The overgrowth of bacteria also upsets the motor activity of the small intestine. Antibiotics may control the condition in the elderly, but surgical resection of diverticula is necessary in younger persons.

Bacterial infections
      Many bacterial organisms can infest the human body and cause disease. Species of Salmonella that cause typhoid (typhoid fever) and paratyphoid (paratyphoid fever) remain endemic scourges in tropical countries and, together with Shigella, are occasional causes of epidemics in institutions, especially among the elderly. Diagnosis is confirmed by the presence of the organisms in a stool culture. Antibiotics and solutions rich in electrolytes are effective therapy. Treatment is with antibiotics. Periodic vaccination is advisable for the protection of individuals exposed to areas where typhoid and paratyphoid are endemic.

       cholera, caused by Vibrio cholerae, is endemic to Southeast Asia and periodically becomes pandemic (widely distributed in more than one country). The oral or intravenous administration of electrolyte solutions rich in potassium has revolutionized the treatment of cholera, because deaths are due to a massive depletion of electrolytes and water. The toxin produced by V. cholerae attaches to the intestinal cells, the enterocytes, where it stimulates the membrane enzyme adenylate cyclase; this in turn interferes with the intracellular enzyme 3′,5′-cyclic adenosine monophosphate synthetase (cyclic AMP), thereby disrupting the sodium pump system for movement of water and allowing potassium and bicarbonate to seep out of the cell.

Parasitic infections
      In tropical countries, parasitism is endemic. Roundworms, tapeworms, amoebae, hookworms, strongyloides, threadworms, and blood flukes (schistosomiasis) are the main types of parasites. Consequently it is commonplace in these areas for multiple parasite infestation to occur in addition to other disorders. This common occurrence, reflecting poverty, lack of health education, malnutrition, contaminated drinking water, and inadequate sanitation, is a major factor in chronic illness and early death.

      Roundworms, particularly Ascaris lumbricoides, may cause intestinal obstruction if present in sufficient numbers. As they mature from the larval state to the adult worm, roundworms migrate through the body, causing ascariasis, an infection characterized by fever, pneumonitis (lung inflammation), cholangitis (inflammation of the bile ducts), and pancreatitis. Roundworms interfere with the absorption of fat and protein in the intestine, causing diarrhea. They are eliminated with the administration of piperazine or other anthelmintics, but occasionally surgery is required for obstruction.

 Hookworm, or Ancylostoma duodenale, infection (hookworm disease) begins when the worm is in the larval stage. It penetrates the skin, usually of the feet, migrates during its life cycle through the liver and the lungs, and attaches to the mucosa of the small intestine where it matures. Hookworms deplete the body of nutrients, and a major effect is severe chronic iron-deficiency (iron deficiency anemia) anemia. This effect can be corrected with the oral administration of iron, and the number of worms can be controlled with tetrachloroethylene or other anthelmintics.

Pinworms (pinworm)
      Pinworms (pinworm), or Enterobius vermicularis, live mainly in the cecum. The adult female migrates at night to the anus and lays eggs on the perianal skin, which cause anal itching. Transmission of the pinworm occurs via a fecal-oral route, and it can affect an entire family. Pinworms can be eradicated with piperazine or vyprinium embonate.

Tapeworms (cestodiasis)
      The common tapeworms are Taenia saginata, found in beef, and T. solium, found in pork. Larvae of Echinococcus granulosus, mature worms of the genus Diphyllobothrium, and some dwarf tapeworms also cause disease. Fertilized ova are passed in feces and are ingested by an intermediary host animal, such as a cow. The embryos migrate to the bloodstream and on reaching muscle or viscera develop into larvae. When the flesh is consumed by humans, the larvae pass into the intestine, where they attach and mature into adult worms. Thus the most common source of infection is inadequately cooked meat. Tapeworms found in beef and pork only give rise to symptoms if their number and size cause intestinal obstruction. Diphyllobothrium latum, a fish tapeworm, may cause a severe anemia similar to pernicious anemia, because it consumes most of the vitamin B12 in the diet of the host.

      Appendicitis is an inflammation of the vermiform appendix that may be caused by infection or partial or total obstruction. The primary symptom of appendicitis is abdominal pain. Appendicitis principally occurs in those younger than 35 years of age. The disorder is easily diagnosed and is treated with surgery. Widespread use of antibiotics for upper-respiratory and other diseases may have lessened the incidence of acute appendicitis, so that more cases of late-developing appendiceal abscess are being reported. Parasitic worms also can contribute to its incidence. Appendicitis occasionally occurs in elderly people, and instances where an abscess forms and bursts require urgent surgery.

Chronic inflammations
      Chronic inflammations of the small intestine include tuberculosis and regional enteritis (enteritis) ( Crohn disease). These disturbances are difficult to diagnose in their early stages because their initial symptoms are often vague. General symptoms include low-grade fever, a tendency toward loose stools, weight loss, and episodes of cramping abdominal pain caused by obstruction of the lumen and interference with normal muscular activity by inflammation of the intestinal wall. Diagnosis is usually determined by X ray or colonoscopy. A biopsy may also be performed to examine the lining of the small intestine. Tuberculosis is treated with specific drug therapy. In Crohn disease anti-inflammatory and immunosuppressive drugs are helpful. Surgical excision of the diseased segments of intestine may be necessary.

      The incidence of Crohn disease is rising. About 60 percent of persons with Crohn disease require surgery because of obstruction of the intestinal lumen and another 20 percent because of fistulation, or connection, between adjacent structures— for example, from the sigmoid colon to the bladder. A combination of repeated surgical excisions from the small intestine and disease of the intestinal wall can result in a severe malabsorptive state. This sometimes requires long-term intravenous nutrition.

Celiac disease
       celiac disease affects between one in 500 and one in 2,000 persons, depending on the region of the world. Celiac disease is caused by damage to the mucosa of the small intestine due to an immune reaction to gluten, a protein present in wheat, rye, barley, and some oats.

      Studies of the immune function of those with celiac disease suggest that at least a major part of the process is a delayed hypersensitivity reaction and that the morphological changes of the small intestine mucosa are correlated with the presence of circulating antibodies to gluten. Damage to the small intestine results in progressive atrophy, if not complete disappearance, of the microvilli and villi that line the intestinal tract. This dramatically reduces the area available for absorption, and malabsorptive diarrhea results. Celiac disease usually occurs between 6 and 24 months of age, but the disorder may not manifest itself until middle age or, if mild, may be unnoticed until then. Iron (iron deficiency anemia) and folic acid deficiency anemias (folic acid deficiency anemia), softening of the bones ( osteomalacia), and general weakness may be accompanied by a variety of disorders attributable to the nonabsorption of vitamins. Untreated, it is a serious though rarely life-threatening disease after infancy. Diagnosis is established by blood tests and biopsy. Withdrawal from the diet of foods that contain gluten generally brings about dramatic improvement and disappearance of all symptoms.

      A malabsorption disorder of unknown cause, tropical sprue affects residents and visitors of tropical countries. It is associated with partial atrophy of the mucosa of the small intestine. Its symptoms are diarrhea, anorexia, and fatigue. If the disease is prolonged, anemia caused by malabsorption of 12 (vitamin B12) develops. Steatorrhea (excess fat in stools) is common, and glucose absorption is impaired. Prolonged treatment with antibiotics, such as tetracycline, and the replacement of vitamins, especially B12 and folic acid, are successful.

      A wide variety of diseases and disorders occur in the large intestine. 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.

       constipation is the delayed passage of waste through the lower portion of the large intestine, with the ultimate discharge of dry, hardened feces from the anus. Constipation may be caused by lack of regularity of one's eating habits and spasms or obstruction of the large intestine. 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. Temporary constipation most often occurs in conjunction with a change or interruption in one's usual activities, as in travel or a change in eating or sleeping habits.

Congenital megacolon
      Aganglionic megacolon, or Hirschsprung disease, is a condition of unknown cause that is characterized by the absence of ganglion cells and normal nerve fibres from the distal (or lower) 3 to 40 cm (1 to 16 inches) of the large intestine. Neuromuscular transmission is absent from this segment, and peristalsis cannot occur. It is thus a functional obstruction. In 10 percent of cases a larger segment is involved and, on rare occasions, the whole colon. The area of normal intestine above the obstruction works harder to push on the fecal contents, and eventually the muscle of the normal segment thickens. The entire colon thus slowly becomes more and more distended and thick-walled. Diagnosis is made by the examination of the microscopic appearance of a deep biopsy of the lower rectum. Various surgical procedures are used to correct the condition.

Acquired megacolon
      Acquired megacolon is commonly caused by a combination of faulty toilet training and emotional disorders during childhood, in which the child withholds defecation. The administration of increasing amounts of laxatives fails to solve the problem permanently, and over time the intrinsic innervation in the intestinal wall is damaged. A dilated rectum full of feces develops over the years. The impacted feces act as an obstruction, and further fecal material piles up behind, with voluminus dilatation of the whole colon in some cases. Evacuation of the contents of the bowel prior to surgery, if it is required, may require hospitalization for up to three months. Acquired megacolon is occasionally encountered in those with schizophrenia and severe depression. It may be related to neurological disorders such as paraplegia, to unrecognized rectal strictures, and to some metabolic disorders. Severe degrees of constipation, often running in families and leading to megacolon, occur, but the cause has not been discovered. Resection of the colon and uniting the ileum to the rectum is effective treatment.

       diarrhea is the abnormally swift passage of waste material through the large intestine, with consequent discharge of loose feces from the anus. Because water is normally absorbed from the colonic content, principally in the ascending, or right, colon, diarrhea can be caused by any inflammatory, neoplastic, or vascular disturbance of that part of the colon. Diarrhea can also be caused by bacterial, viral, or parasitic infection. Most cases of diarrhea are not serious and do not require treatment.

      Diarrhea is common in those who are deficient in lactase, the enzyme that splits lactose (milk sugar) into its component parts, glucose and galactose. Shortly after drinking milk, such persons usually have severe intestinal cramping, followed later by watery diarrhea. The lactose in the milk is not broken down, and it stays in the lumen of the small intestine, drawing water to it. The increased bulk of fluid and sugar distends the intestine, which then contracts actively. The rapid contractions drive the material along the intestine into the colon, which cannot absorb the water rapidly enough. The resultant watery, unformed stools are frequently acidic.

Intestinal gas
       intestinal gas consists principally of swallowed air and partly of by-products of digestion. When a person is in an upright position, gas diffuses to the uppermost portions of the colon. There it is compressed by the contraction of adjacent segments, giving rise to pain that is localized either near the liver and gallbladder or under the diaphragm and heart. This pain can be incorrectly thought to be associated with diseases of these organs, whereas it is actually caused by increased gas in the colon. Eating slower to reduce the amount of air ingested, decreasing the intake of carbonated beverages and whipped foods that contain air bubbles, and avoiding certain gas-producing foods, such as most beans, onions, sprouts, nuts, and raisins, usually help to reduce flatulence.

      Diverticula (diverticulum) are small pouches or sacs that form in the wall of the large intestine. Arteries penetrate the muscular walls of the colon from its outside covering, the serosa, and distribute themselves in the submucosa. With aging, and perhaps in persons predisposed to the disorder, the channels in which these arteries lie become larger. If the peristaltic activity of the colon maintains a high pressure within its lumen, as in persons straining to defecate, the mucous membrane of the colon may be driven slowly into these channels and eventually may follow the arteries back to their site of colonic entrance in the serosa. At this time, the outward-pushing mucosa becomes a budding sac, or diverticulum, on the antimesenteric border of the colon with a connection to the lumen. In the Western world, multiple colonic diverticula occur in as many as 30 percent of persons older than 50 years. Diverticula are particularly common in those whose diets are deficient in fibre. Hypertrophy (increase in size and mass) of the muscle fibre of the colon, especially in the sigmoid region, precedes or accompanies diverticulosis; this is especially apparent in the diverticulosis in middle-aged persons as opposed to that in the elderly.

      The principal dangers of diverticulosis are hemorrhage and inflammation. Hemorrhage results from the action of hard stools against the small arteries of the colon that are exposed and unsupported because of diverticula. As the arteries age, they become less elastic, less able to contract after bleeding begins, and more susceptible to damage. Diverticulitis occurs when the narrow necks of the diverticula become plugged with debris or undigestible foodstuff and when bacteria, uninhibited by the usual motor activity that keeps the intestine clean, proliferate in the blind sacs. When the sacs enlarge, the adjacent intestinal wall becomes inflamed and irritable, muscle spasms occur, and the patient experiences abdominal pain and fever. If the sacs continue to enlarge, they may rupture into the peritoneum, giving rise to peritonitis, an inflammation of the peritoneum. More commonly they fix themselves to neighbouring organs and produce localized abscesses, which may prove difficult to treat surgically. Mild diverticulitis responds well to antibiotics; massive hemorrhages often require emergency surgery. Recurrent diverticulitis requires resection of the affected area of the colon.

Abscesses (abscess)
      Abscesses (cavities of pus formed from disintegrating tissue) in the perianal area are common complicating features of many diseases and disorders of the large intestine. Fungal infections of the moist and sometimes poorly cleansed area around the anus are common and permit the maceration (or gradual breaking down) of tissue and invasion by bacteria from the skin and colon. In diabetics, who are susceptible to skin infection, perianal hygiene is very important.

Bacterial (bacteria) infections
      The colon may become inflamed because of invasion by pathogenic, or disease-causing, bacteria or parasites. A variety of species of Shigella, for example, attack the mucous membrane of the colon and produce an intense but rather superficial hemorrhage. In infants and in the elderly, the amount of fluid and protein lost by the intense inflammatory response may be fatal, but ordinarily such symptoms are less serious in otherwise healthy persons. Salmonella species, responsible for severe generalized infections originating from invasion of the small intestine, may damage the lymph follicles of the colon, but they do not produce a generalized inflammation of the colon (colitis (ulcerative colitis)). The cytomegalic virus, on the other hand, can cause a severe colitis, producing ulcerations. Lymphopathia venereum causes a more generalized and superficial colitis.

      Food residues provide an excellent culture medium for bacteria, and the interior of the colon is a nearly ideal environment for their growth. The most widely distributed parasite producing disease in the colon is the protozoan Entamoeba histolytica. This parasite enters the digestive tract via the mouth and lodges in the cecum and ascending colon. This usually results in irritability of the ascending colon and failure to absorb water properly, so that intermittent, watery diarrhea ensues. The amoebas undermine the mucosal coat and may create large ulcerations that bleed excessively. Stools contain blood, but there is little pus or other evidence of reaction by the colon to the invading organism. In more generalized amoebic colitis, the rectum and sigmoid colon are invaded by E. histolytica, which manifest their presence by numerous discrete ulcerations separated from each other by a relatively normal-appearing mucous membrane. The amoebas may enter the portal circulation and be carried to the liver, where abscesses form and sometimes rupture into the chest or the abdominal cavity. Immunologic tests of the blood may help in diagnosis. After identification of the parasites by direct smear tests from the margin of the ulcers or from the stools, a combination of amoebicidal drugs and a broad-spectrum antibiotic—i.e., an antibiotic that is toxic to a wide variety of parasites, usually metronidazole and tetracycline—is administered.

      The most common form of chronic colitis (inflammation of the colon) in the Western world, ulcerative colitis, is idiopathic (i.e., of unknown cause). Ulcerative colitis varies from a mild inflammation of the mucosa of the rectum, giving rise to excessive mucus and some spotting of blood in the stools, to a severe, sudden illness, with destruction of a large part of the colonic mucosa, considerable blood loss, toxemia and, less commonly, perforation. The most common variety affects only the rectum and sigmoid colon and is characterized by diarrhea and the passage of mucus. Ulcerative colitis tends to follow a remitting-relapsing course. Diagnosis is determined by performing a colonoscopy or a biopsy.

      Another type of colitis arises when antibiotic use causes the abnormal proliferation of certain types of bacteria in the colon, leading to inflammation. This disorder is treated by stopping the use of the causal antibiotic and administering others such as vancomycin or mexronidazole. About 15 percent of all cases of colitis involve extension of the disease beyond the area initially affected, with an increase in severity. Where the destruction has been extensive, there is a risk of malignancy 10 to 20 years after the onset of the disease.

      Crohn disease is characterized by chronic inflammation of the digestive tract, usually the terminal portion of the small intestine. The cause of Crohn disease is unknown. Apart from the greater tendency for fistulas to form and for the wall of the intestine to thicken until the channel is obstructed, it is only distinguishable from ulcerative colitis by microscopic findings. In Crohn disease, the maximum damage occurs beneath the mucosa, and lymphoid conglomerations, known as granulomata, are formed in the submucosa. Crohn disease attacks the perianal tissues more often than does ulcerative colitis. Although Crohn disease and ulcerative colitis are not common, they are disabling.

      A combination of immunosuppressive and anti-inflammatory drugs, including corticosteroids and aminosalicylic acid compounds, are used to treat Crohn disease. The drugs are effective both in treating acute episodes and in suppressing the disease over the long term. Depending on the circumstances, hematinics, vitamins, high-protein diets, and blood transfusions are also used. Surgical resection of the portion of the large bowel affected is often performed. The entire colon may have to be removed and the small intestine brought out to the skin as an ileostomy, an opening to serve as a substitute for the anus. In ulcerative colitis, as opposed to Crohn disease, the rectal muscle may be preserved and the ileum brought through it and joined to the anus.

      In the Western world, colon cancer (colorectal cancer) is more common than is stomach cancer, and it occurs about equally in both sexes. Risk factors for colon cancer include age, diets that are high in fat and low in fibre, a personal or family history of cancer, and the presence of polyps or ulcerative colitis. Symptoms are highly variable, the main feature being blood in the stools, but this may be detectable only by chemical testing. Cancers compress the colonic lumen to produce obstruction, they attach to neighbouring structures to produce pain, and they perforate to give rise to peritonitis. Cancers also may metastasize to distant organs before local symptoms appear. Nevertheless, the prognosis for patients with this cancer is considerably better than it is for cancer of the stomach. Some patients require a colostomy, in which an opening is made from the colon to the skin, where the fecal contents are extruded. After the colon has been removed partially, it is possible to join the terminal ileum or the remnant colon directly to the anal canal. A reservoir also can be fashioned out of the terminal ileum and placed inside the rectum muscle from which the inflamed mucosa has been removed. This functions as a normal rectum, and with retained sphincters at the anus, can render the patient continent, although there usually are three or four bowel movements daily.

Polyps (polyp)
      The tendency of some persons to form polyps, benign growths on the inner wall of the colon, is strikingly exemplified in the rare disorder known as familial polyposis, in which the colon may be studded with hundreds or thousands of small polyps. Because a colon that produces so many polyps eventually produces cancers as well, the colon should be removed surgically as soon as the diagnosis is made. The rectum may be left, but a visual examination of the residual mucosa must be made twice yearly to detect signs of early cancerous change. Another peculiar form of polyp is the villous adenoma, often a slowly growing, fernlike structure that spreads along the surface of the colon. It can recur after being locally resected, or it can develop into a cancer.

Anal disorders
      Anorectal (anal canal) disorders related to defecation are more common in the Western world than elsewhere. Whether this distribution is related to diet, exercise, or personal hygiene is not clear. These disorders usually take the form of fissures (cuts or cracks in the skin or mucous membrane) at the junction of the anal mucous membrane with the skin between the thighs. If such fissures become chronically infected and resistant to treatment by sitz baths and local medication, they may require surgical correction. Anal fistulas sometimes occur as complications of serious bowel disease, as in tuberculosis or Crohn disease of the bowel, or in certain parasitic diseases. A more general disorder is the enlargement of veins of the rectum and anus to form external or internal hemorrhoids (hemorrhoid). Many adults in the Western world have such venous enlargements, but only a small number suffer serious symptoms from their presence. Hemorrhoids protrude, are associated with anal itching and pain, and bleed, especially when they come in contact with hard stools. These symptoms generally can be controlled by conservative measures, but occasionally they persist or cause so much distress that surgical removal of the enlarged and dilated veins is necessary.

fred Sircus

      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: the hepatocyte (liver cell), 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 to damaged canaliculi, small channels that transport bile from hepatocytes.

      Most acute liver diseases are self-limiting, and liver function 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. For example, 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), healthy tissue is 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 cytomegalovirus and Epstein-Barr virus, which causes infectious mononucleosis (mononucleosis), there are three distinctive transmissible viruses that are specifically known to cause acute damage to liver cells: hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis C virus (HCV).

      The hepatitis A virus is transmitted almost exclusively via the fecal–oral route, and it thrives in areas where sanitation and food handling are poor and hand washing is infrequent. HAV 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 HAV for several months with either the hepatitis A vaccine or a single injection of immunoglobulin. 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.

      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 signs 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. 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 secretions 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.

      Hepatitis C appears to be transmitted in a manner similar to HBV transmission. The incidence for HCV is high among persons engaging in promiscuous sexual activity, intravenous drug users, homosexual males, children living in endemic areas, infants born to infected mothers, health care workers, and hemodialysis patients. The average incubation period of the disease is about seven weeks, and an acute attack of hepatitis C is usually less severe than acute hepatitis B. Hepatitis C, however, is more likely to become chronic than is hepatitis B, and it may recur episodically with acute flares. The two approved treatments for hepatitis C are alpha interferon and ribavirin; only about half of those receiving the drugs respond to them.

      The symptoms characteristic of acute hepatitis caused by HAV, HBV, and HCV are essentially similar. Patients often complain of a flulike illness for several days, with chills, fever, headache, cough, nausea, occasional diarrhea, and 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 antigen-antibody complexes in the small blood vessels of adjacent organs. After several days 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. 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 a 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 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 7 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 except liver transplantation.

      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 is beyond the capacity of the hepatocyte to conjugate, or join them with another substance for detoxification and excretion.

Acute canalicular (cholestatic) hepatitis
      Acute canalicular (cholestatic) hepatitis is most commonly caused by certain drugs, such as psychopharmacologics, antibiotics, and anabolic steroids or, at times, by hepatitis viruses. The symptoms are generally those of biliary obstruction and include itching, jaundice, and light-coloured stools. Drug-induced cholestasis almost invariably disappears within days or weeks after exposure to the agent is discontinued. Acute congestive liver disease usually results from the sudden engorgement of the liver by fluids after congestive heart failure (heart failure). The liver may enlarge and become tender. The levels of hepatocytic enzymes in the blood are often greatly increased, and recovery is rapid once the heart failure improves. Jaundice is uncommon in acute hepatic congestion.

Chronic active hepatitis
      Chronic hepatitis is the result of unresolved acute injury and is associated with ongoing liver damage. The course of the disease is usually slow but relentlessly progressive. A milder form of chronic disease, called persistent hepatitis, does not appear to lead to progressive liver damage despite evidence of a continuing mild inflammation. These conditions may result from viral hepatitis, drug-induced hepatitis, autoimmune liver diseases (lupoid hepatitis), or congenital abnormalities. A prominent autoimmune liver disease is Wilson disease, which is caused by abnormal deposits of large amounts of copper in the liver. Granulomatous hepatitis, a condition in which localized areas of inflammation (granulomas) appear in a portion of the liver lobule, is a type of inflammatory disorder associated with many systemic diseases, including tuberculosis, sarcoidosis, schistosomiasis, and certain drug reactions. Granulomatous hepatitis rarely leads to serious interference with hepatic function, although it is often chronic.

      Chronic viral hepatitis B and C can be treated with interferon. cirrhosis of the liver, and occasionally liver cancer, usually result from a gradual loss of liver function. Chronic hepatitis that is the result of autoimmune disorders usually responds to the administration of immunosuppressive medications and adrenal corticosteroids, which moderate the inflammatory reaction.

      The end result of many forms of chronic liver injury is cirrhosis, or scarring of liver tissue in response to previous acinar necrosis and irregular regeneration of liver nodules and bile ducts. Among the congenital disorders producing cirrhosis are Wilson disease, hemochromatosis (over-deposition of iron pigment), cystic fibrosis, biliary atresia (congenital absence of a part of the bile ducts), and alpha1-antitrypsin deficiency, or the congenital absence of a proteolytic enzyme inhibitor that results in the accumulation of abnormal forms of carbohydrate in hepatocytes. In the Western world, cirrhosis of the liver most commonly results from chronic heavy intake of alcohol (alcoholism). This type of cirrhosis is known as Laënnec, or portal, cirrhosis. Chronic viral hepatitis is probably the leading cause of cirrhosis in underdeveloped countries. Primary biliary cirrhosis, a geographically widespread, though uncommon, autoimmune inflammatory disease of bile ducts, is a disorder primarily affecting middle-aged and older women. The inflammation leads to necrosis and gradual disappearance of bile ducts over a period of one or more decades. Secondary biliary cirrhosis results from chronic obstruction or recurrent infection in the extrahepatic bile ducts caused by strictures, gallstones (gallstone), or tumours (tumour). Infestation of the biliary tract with a liver fluke, Clonorchis sinensis, is a cause of secondary biliary cirrhosis in Asia. Cirrhosis occasionally is the result of chronic vascular congestion of the liver in persons with prolonged heart failure and in those with chronic obstruction of the hepatic veins caused by benign blood clots or metastatic cancer.

      Symptoms of cirrhosis are usually absent during the early stages of the disease. Occasionally, cirrhosis is detected during a physical examination when an enlargement of the liver, spleen, or veins in the upper abdominal wall is found. More often, patients develop symptoms related either to the failure of the liver to perform its functions or to complications caused by the circulatory changes that a cirrhotic liver imposes on the venous blood flow from the intestinal tract (portal hypertension). Thus, common symptoms of cirrhosis include jaundice, resulting from reduced passage of conjugated bilirubin into the biliary tract; increased bleeding, from sequestration of blood platelets in a congested spleen; or deficient production of short-lived coagulation proteins by the liver. There may be certain changes in the skin, such as the appearance of small spiderlike vascular lesions on the hands, arms, or face, a marked reddening of portions of the palms, or enlargement of the breast in females or reduction in testicular size in males. These symptoms are believed to occur because of the liver's inability to metabolize the female sex hormones normally produced by the body. The gradual accumulation of fluid in the abdominal cavity (ascites), sometimes accompanied by swelling of the ankles, is attributable to portal hypertension and to reduced hepatic production of albumin, while failure of the liver to metabolize amino acids and other products of protein digestion may lead to the state of confusion called hepatic encephalopathy. Loss of appetite, reduction of muscle mass, nausea, vomiting, abdominal pain, and weakness are other symptoms of hepatic cirrhosis. Diabetes (diabetes mellitus) in a patient with cirrhosis is frequently caused by hemochromatosis (excessive deposition of iron in tissues, especially in the liver and pancreas), since iron deposits compromise the production of insulin by the islets of Langerhans in the pancreas. Severe spastic disorders of the muscles in the limbs, head, and face suggest the presence of Wilson disease, especially if there is a family history, since the copper deposits characteristic of that disorder are toxic to the liver and to structures in the base of the brain. A history of chronic lung infections or of progressive obstructive lung disease may be present in patients with cystic fibrosis or a deficiency of alpha1-antitrypsin.

      A diagnosis of cirrhosis is confirmed by blood tests that show an elevated concentration of hepatocytic enzymes, reduced levels of coagulation proteins, elevated levels of bilirubin, and, most important, reduced amounts of serum albumin (a major protein of human blood plasma) and increases in serum globulin (a specific group of proteins found in blood plasma and including immunoglobulins). Although other tests may also be abnormal in patients with acute liver disease, serum albumin levels are usually not reduced in the acute stage of the disease because that protein is rather long-lived (up to one month) and levels do not decrease until the liver disease becomes chronic. Elevated levels of serum iron or copper support a diagnosis of hemochromatosis or Wilson disease, respectively, while a positive test for serum antibodies to cellular mitochondria is associated almost solely with primary biliary cirrhosis. The presence of HBV surface antigen or of delta agent suggests viral cirrhosis. A biopsy of the liver is the most valuable diagnostic test, since this procedure makes available an actual specimen of liver tissue for microscopic examination. Treatment of cirrhosis of the liver never results in a completely normal organ, since the process of scarring and nodular regeneration is permanent. The process itself, however, can be prevented or its progress halted by managing the precipitating factors of the disease.

Complications of advanced liver disease
Hepatic encephalopathy
      Hepatic encephalopathy refers to changes in the brain that occur in patients with advanced acute or chronic liver disease. If liver cells are damaged, certain substances that are normally cleansed from the blood by the healthy liver are not removed. These products of cell metabolism are primarily nitrogenous substances derived from protein, especially ammonia, or possibly certain short-chain fatty acids. They pass to the brain where they damage functioning nervous tissue or subvert the actions of neurotransmitters, chemical messengers that carry impulses from one brain cell to another. In acute cases, the brain becomes swollen to the point where normal breathing may cease. Chronic exposure can lead to destruction of nerve cells with replacement by scar tissue (gliosis). A patient with chronic hepatic encephalopathy may develop progressive loss of memory, disorientation, and muscular tremors, leading to a form of chronic dementia. The ingestion of protein invariably aggravates these symptoms. Patients with gastrointestinal bleeding, infection, kidney failure, and constipation and those who are taking certain medications are all at risk of worsened episodes of hepatic encephalopathy.

      The treatment of hepatic encephalopathy involves, first, the removal of all drugs that require detoxification in the liver and, second, the reduction of protein intake. ammonia is a potentially harmful by-product of digestion, and its concentration in the blood can be lowered either through the reduction of intestinal bacteria by administration of enteric antibiotics, which reduce the production of ammonia in the colon or by administration of lactulose, a nonabsorbable carbohydrate whose by-products make the contents of the colon more acidic, creating an environment that reduces the diffusion of ammonia from the intestinal lumen to the portal blood vessels.

Portal hypertension
      Portal hypertension is the increased pressure in the portal vein and its tributaries. It is the result of impediments to venous flow into the liver, and is brought about by the scarring characteristic of the cirrhotic process. The increased pressure causes feeders of the portal vein to distend markedly, producing varices, or dilations of the veins. When varices are located in superficial tissues, they may rupture and bleed profusely. Varices most commonly occur in the lower esophagus, the stomach, and the perianal region. Esophageal varices are likely to bleed most heavily, and, because of the reduced blood flow in the liver that results and the large amount of protein contained in the blood that is shed into the intestines, profuse bleeding from esophageal varices is frequently associated with the onset of hepatic encephalopathy or coma. Because of their location at the lower end of the esophagus or the upper portion of the stomach, bleeding from varices is often difficult to control. Bleeding may stop spontaneously, but it is likely to recur. Considerable success in stemming such hemorrhage and preventing its recurrence has been achieved by using rubber bands to block the blood supply to each varix or by the injection of sclerosing (hardening) agents into varices during endoscopic visualization. If variceal bleeding persists and if the patient can withstand a long and complex operative procedure, surgical formation of a shunt, or artificial passageway, from the portal vein or one of its feeders to a systemic abdominal vein, such as the vena cava or the left renal vein, or from the hepatic vein to the portal vein may be performed.

      The accumulation of fluid in the abdominal cavity, or ascites, is related to portal hypertension, significant reduction in serum albumin, and renal retention of sodium. When albumin levels in the blood are lower than normal, there is a marked reduction in the force that holds plasma water within the blood vessels and normally resists the effects of the intravascular pressure. The resulting increase in intravascular pressure, coupled with the increased internal pressure caused by the portal venous obstruction in the liver, leads to massive losses of plasma water into the abdominal cavity. The associated reduction of blood flow to the kidneys (kidney) causes increased elaboration of the hormone aldosterone, which, in turn, causes the retention of sodium and water and a reduction in urinary output. In addition, because the movement of intestinal lymph into the liver is blocked by the cirrhotic process in the liver, the backflow of this fluid into the abdominal cavity is greatly increased. The volume of abdominal ascites in adults with cirrhosis may reach levels as great as 10 to 12 litres (11 to 13 quarts). Ascitic fluid may accumulate in the scrotum and in the chest cavity, where its presence, combined with the upward pressure on the diaphragm from the abdominal fluid, may severely affect breathing. Appetite also is often reduced by the abdominal distention.

      The treatment of cirrhotic ascites begins with the removal of enough fluid directly from the abdomen by needle puncture to ease discomfort and breathing. Patients are placed on diets low in salt (sodium chloride), and they are given diuretic drugs to increase the output of water by the kidneys. If these measures do not control massive ascites, ascites can be drained internally into the general venous blood system by running a plastic tube from the abdominal cavity, under the skin of the chest, into the right internal jugular vein of the neck (peritoneovenous shunt of LeVeen) or from the hepatic vein to the portal vein.

Hepatorenal syndrome
      Hepatorenal syndrome, a progressive reduction in kidney function that often occurs in persons with advanced acute or chronic liver disease, probably results from an inadequate flow of blood through the cortical (outer) portions of the kidneys, where most removal of waste products occurs. In some instances, hepatorenal syndrome is caused by marked reductions in blood volume that result from a low concentration of water in the blood. Hemorrhages also can reduce kidney function by leading to damage of renal tubules. Finally, with advanced hepatocytic dysfunction, a spasm of blood vessels in the renal cortex can occur, which results in progressive failure in kidney function and often leads to death. The kidneys themselves are frequently undamaged structurally. Treatment of patients with volume depletion and tubular damage often may lead to significant improvement in kidney function. Dialysis may improve symptoms.

Tumours (tumour)
       liver cancer, usually in hepatocytes and less frequently in cells of bile duct origin, is rare in the Western world and is almost always associated with active cirrhosis, particularly the form found in patients with chronic hepatitis. The survival rate from liver cancer is low. In certain underdeveloped countries, especially in Africa, the incidence of this malignancy is high and is a major cause of death in the population. Most of these cases appear to stem from the prevalence of chronic viral hepatitis or the chronic presence of viruses in the blood (viremia) caused by hepatitis B. Long exposure to certain environmental poisons, such as vinyl chloride or carbon tetrachloride, has also been shown to lead to hepatic cancer.

      Cancers arising elsewhere in the body, particularly in abdominal organs, lungs, and lymphoid tissue, commonly lead to metastatic cancer in the liver and are by far the most frequent type of hepatic malignancy. Usually, when such metastases are found, the primary tumour has advanced beyond the stage where it can be removed surgically.

      Various benign types of tumours and cysts arise from certain components of the liver, such as the hepatocytes (adenomas) or blood vessels (hemangiomas). While the cause of these lesions is not always clear, hepatic adenomas are associated with the prolonged use of female sex hormones (estrogens). Symptoms of benign tumours depend mainly on their size and their position in relation to the surface of the liver. If they enlarge significantly, patients may experience pain or sensations of heaviness in the upper abdomen. When benign tumours are located close to the surface of the liver, they may rupture through the capsule and bleed freely into the abdominal cavity. Surgery is then required.

      Benign cysts (cyst) (tissue swellings filled with fluid) in the liver may occur as congenital defects or as the result of infections from infestation of the dog tapeworm (Echinococcus granulosus). Abscesses (abscess) on the liver result from the spread of infection from the biliary tract or from other parts of the body, especially the appendix and the pelvic organs. Specific liver abscesses also result from infections with the intestinal parasite Entamoeba histolytica. Abscesses usually respond well to treatment with specific antibiotics, although surgical drainage is required in some cases.

Biliary tract

      Cholelithiasis, or the formation of gallstones (gallstone) in the gallbladder, is the most common disease of the biliary tract. Gallstones are of three types: stones containing primarily calcium bilirubinate (bilirubin) (pigment stones); stones containing 25 percent or more of cholesterol (cholesterol stones); and stones composed of variable mixtures of both bilirubin and cholesterol (mixed gallstones).

      Pigment stones are more common in certain parts of Asia than in the Western world, and they usually occur in persons who have 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 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 stasis (stagnation of blood). The reasons for the increased incidence of pigment stones among persons with cirrhosis of the liver and the elderly 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 stones occur when the proportion of cholesterol in bile exceeds the capacity of bile acids and the phospholipid 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, such as Crohn disease, 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. Decreased flow of bile in the gallbladder, a condition that occurs late in pregnancy, in persons on diets low in fat, and among 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 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 upper 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 shaking chills, with high, spiking fevers (fever). 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.

      Gallstones are easy to diagnose since canaliculi, small channels, 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.

      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. 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.

      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 drugs made from bile acids called urosodiol and chenodiol. The ingestion of these medications 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 structure, including the gallbladder, the hepatic ducts, the common bile duct, or the hepatopancreatic ampulla (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). Congenital cysts and parasitic infections, such as liver flukes, seem to lead to increased risk of cancer of the bile duct. Persons with extensive chronic ulcerative colitis or primary sclerosing cholangitis 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 cure rate is low. 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 is characterized by painful attacks, often resembling preoperative symptoms, that occasionally occur following the surgical removal of gallstones and the gallbladder. These attacks may be related to biliary stricture, gallstones (gallstone), or intermittent muscular spasms of the sphincter of Oddi (hepatopancreatic sphincter). Drugs are used to help prevent or reduce symptoms.

       jaundice, or yellowing of the skin, sclera (outer layer of the eyeball), and mucous membranes, occurs whenever the level of bilirubin in the blood is significantly above normal. This condition is evident in three different types of disorders, more than one of which may be present simultaneously in a single person. The first type, unconjugated, or hemolytic, jaundice, appears when the amount of bilirubin produced from hemoglobin by the destruction of red blood cells or muscle tissue (myoglobin) exceeds the normal capacity of the liver to transport it or when the ability of the liver to conjugate normal amounts of bilirubin into bilirubin diglucuronide is significantly reduced by inadequate intracellular transport or enzyme systems. The second type, hepatocellular jaundice, arises when liver cells are damaged so severely that their ability to transport bilirubin diglucuronide into the biliary system is reduced, allowing some of this yellow pigment to regurgitate into the bloodstream. The third type, cholestatic, or obstructive jaundice, occurs when essentially normal liver cells are unable to transport bilirubin either through the capillary membrane of the liver, because of damage in that area, or through the biliary tract, because of anatomical obstructions (closure or absence of an opening, gallstones (gallstone), cancer).

Unconjugated jaundice
      Unconjugated, or hemolytic, jaundice is characterized by the absence of bile pigments in the urine and by normal stool colour. The colour of the urine is normal because the bilirubin in the blood is unconjugated to glucuronic acid and therefore bound to blood albumin and insoluble in water. Thus the bilirubin is not filtered by the kidneys. The colour of stools remains normal because much of the bilirubin in the blood is filtered normally by the liver and enters the intestine promptly by way of the biliary system. Hemolytic diseases in newborns may lead to serious brain damage ( kernicterus) if the unconjugated bilirubin crosses into the brain stem and destroys vital nuclei. The exposure to blue light of infants at risk for kernicterus converts the bilirubin to harmless and colourless degradation products. Unconjugated hyperbilirubinemia also occurs in many newborns, especially if they are premature, when the bilirubin transport enzyme systems are not fully developed. This disorder is self-limited, may require occasional exposures to blue light, and usually disappears within the first two weeks of extrauterine life. Gilbert disease, a fairly common hereditary deficiency in the hepatic transport protein ligandin and the conjugating enzyme glucuronyl transferase, results in a harmless lifelong tendency to mild degrees of unconjugated jaundice, especially during periods of fasting or fatigue.

Hepatocellular jaundice
      Hepatocellular jaundice, present in all types of hepatitis and cirrhosis and in congestive liver disease, is characterized by dark amber urine and normal or slightly paler than normal stools. Because much of the bilirubin in the blood already has been conjugated by the endoplasmic reticulum of the hepatocyte, it is water-soluble and can be filtered by the kidneys. Stools are usually normal because some bile pigment also manages to be excreted into the biliary tract and intestine.

Cholestatic jaundice
      Cholestatic jaundice is also distinguished by amber-coloured urine, but the colour of the stools is likely to be very pale (clay-coloured) due to the failure of bile pigments to pass into the intestine. Itching of the skin is commonly associated with this condition. Cholestasis occurs in many types of hepatitis, especially those caused by certain drugs, and in diseases that primarily damage small bile passages in the liver (intraheptic cholestasis). Cholestatic jaundice also occurs in patients with obstructive disorders of the biliary tract outside of the liver (extrahepatic cholestasis). It is often impossible to determine the level of obstruction by means of examination alone, and more sophisticated imaging techniques are required to locate the site of damage.

      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 to the pancreas, certain drugs, viral infections, heredity, hyperlipidemia (increased levels of blood fats), and congenital deformities of the ductal system. In the Western world most cases are related either to alcoholism or to gallstones (gallstone), especially when stones pass spontaneously into the hepatopancreatic ampulla (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 pancreas, which allows the escape of activated and destructive digestive enzymes (enzyme) into the substance of the pancreas itself and into surrounding tissues. Overstimulation of secretory enzyme production mechanisms in the acinar cell may also lead to the activation 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 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 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 levels. Ultrasonographic or computed tomographic (CT) 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 sodium 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 (gallstone), cessation of alcohol consumption, a low-fat diet, and discontinuation of toxic drugs (thiazide diuretics, immunosuppressives, and corticosteroids, 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 decrease the number of further attacks.

Chronic pancreatitis
      Chronic pancreatitis rarely follows repeated acute attacks. It seems instead to be a separate disorder that can result from 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 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 the Western world. Chronic protein malnutrition is a primary cause 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 oral pancreatic enzyme supplements to correct dietary malabsorption.

Cystic fibrosis
       cystic fibrosis is inherited, but it is not expressed unless both members of a pair of homologous, or corresponding, chromosomes carry the trait. The major functional abnormality in persons with the disease appears to be the elaboration by mucous glands throughout the body of secretions containing greater than normal concentrations of protein and calcium. This imbalance leads to increased viscosity of the secretions of mucus and organic constituents in gland ducts. The resulting plugging process in the pancreas almost invariably causes destruction and scarring of the acinar tissue, usually without damaging the islets of Langerhans. A similar process in the hepatic biliary system produces a form of cirrhosis. In cystic fibrosis, the resulting pancreatic insufficiency usually can be treated by the oral replacement of pancreatic enzymes.

       pancreatic cancer arises primarily from the ductal system of the pancreas. The incidence of pancreatic cancer has increased slightly (somewhat more in men than in women) and now exceeds cancer of the stomach. Risk factors include age, race, gender, a diet high in fat, smoking, diabetes (diabetes mellitus), family history, exposure to pesticides, certain dyes and chemicals, ulcers (ulcer), and chronic pancreatitis. Upper abdominal pain, often radiating to the back, and weight loss are the most common symptoms of pancreatic cancer. Obstructive jaundice is a frequent symptom when the head of the pancreas is involved. The diagnosis is readily made in most cases by CT scan, at times supplemented by biopsy. There is no effective treatment. If the tumour is localized and has not invaded blood vessels and nerves surrounding the pancreas, it occasionally can be removed surgically. Jaundice and intestinal obstruction can be relieved temporarily by surgical bypass procedures. Radiation and chemotherapy have shown some promise as therapeutic agents if they are started promptly in the course of the disease and are continued for long periods.

Harvey J. Dworken

Additional Reading
Gastrointestinal diseases are discussed in such works as Eugene R. Schiff, Michael F. Sorrell, and Willis C. Maddrey (eds.), Schiff's Diseases of the Liver, 8th ed., 2 vol. (1999); Robert F. Service, “Stalking the Start of Colon Cancer,” Science, 263(5153):1559–60 (March 18, 1994); Martin J. Blaser, “The Bacteria behind Ulcers,” Scientific American, 274(2):104–107 (February 1996); Joseph Alper, “Ulcers as an Infectious Disease,” Science, 260(5105):159–160 (April 9, 1993); Charles Herbert Best and Norman Burke Taylor, Best and Taylor's Physiological Basis of Medical Practice, 12th ed., edited by John B. West (1991); 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, Sleisenger & Fordtran's Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management, 6th ed., edited by Mark Feldman, Marvin H. Sleisenger, and Bruce F. Scharschmidt, 2 vol. (1998); David J.C. Shearman, Niall Finlayson, and Michael Camilleri (eds.), Diseases of the Gastrointestinal Tract and Liver, 3rd ed. (1997); H.L. Duthie (ed.), Gastrointestinal Motility in Health and Disease (1978); William S. Haubrich and Fenton Schaffner, Bockus Gastroenterology, 5th ed., edited by J. Edward Berk, 4 vol. (1994); and Franklin Bicknell, Vitamins in Medicine, 4th ed., edited by Brian M. Barker and David A. Bender, 2 vol. (1980–82). Information on current research is available in Fred Kern and A.L. Blum (eds.), Gastroenterology Annual.

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Universalium. 2010.

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