Diseases and Disorders of the Digestive System

Peritonitis

Peritonitis is an inflammation of the peritoneum, usually caused by an infectious organism that is introduced into the abdominal cavity.

Learning Objectives

Describe the causes and prognosis of peritonitis

Key Takeaways

Key Points

  • Perforation of part of the gastrointestinal tract is the most common cause of peritonitis.
  • The main manifestations of peritonitis are acute abdominal pain, abdominal tenderness, and abdominal guarding.
  • Depending on the severity of the patient’s state, the management of peritonitis may include supportive measures, antibiotics, or surgery.
  • If properly treated, typical cases of surgically correctable peritonitis (e.g., perforated peptic ulcer, appendicitis, and diverticulitis ) have a mortality rate of less than 10%.

Key Terms

  • Spontaneous bacterial peritonitis (SBP): Spontaneous bacterial peritonitis (SBP) is the development of peritonitis (infection in the abdominal cavity) despite the absence of an obvious source for the infection.
  • peritoneal dialysis: A treatment for patients with severe chronic kidney disease in which fluids are exchanged from the blood in the patient’s peritoneum in the abdomen.
  • Blumberg sign: Blumberg’s sign is a sign that is elicited during physical examination in medicine and is indicative of peritonitis. A positive sign shows rebound tenderness, meaning that pressing a hand on the abdomen elicits less pain than releasing the hand abruptly, which will aggravate the pain, as the peritoneum snaps back into place.

Peritonitis is an inflammation of the peritoneum, the thin tissue that lines the inner wall of the abdomen and covers most of the abdominal organs. Peritonitis may be localized or generalized, and may result from infection (often due to rupture of a hollow organ as may occur in abdominal trauma or appendicitis) or from a non-infectious process.

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Peritoneum: The peritoneum, colored in blue, is the serous membrane that forms the lining of the abdominal cavity. It covers most of the intra-abdominal, supporting them and serving as a conduit for their blood and lymph vessels and nerves. Peritonitis is an inflammation of the peritoneum often causing abdominal pain and tenderness.

Symptoms and Complications

The main manifestations of peritonitis are acute abdominal pain, abdominal tenderness, and abdominal guarding, which are exacerbated by moving the peritoneum by coughing, flexing one’s hips, or eliciting the Blumberg sign. Diffuse abdominal rigidity (“washboard abdomen”) is often present, especially in generalized peritonitis. Other symptoms include fever, sinus tachycardia, and development of intestinal paralysis, which also causes nausea, vomiting, and bloating.

Complications of peritonitis include sequestration of fluid and electrolytes, as revealed by decreased central venous pressure, which may cause electrolyte disturbances, as well as significant hypovolemia, possibly leading to shock and acute renal failure. A peritoneal abscess may form and sepsis may develop, so blood cultures should be obtained.

Causes

Perforation of part of the gastrointestinal tract is the most common cause of peritonitis. Examples include perforation of the distal esophagus, of the stomach by a peptic ulcer or gastric carcinoma, of the duodenum, of the remaining intestine by appendicitis, diverticulitis, inflammatory bowel disease (IBD), intestinal infarction, intestinal strangulation, colorectal carcinoma, or of the gallbladder. Other possible reasons for perforation include abdominal trauma, ingestion of a sharp foreign body (such as a fish bone, toothpick or glass shard), perforation by an endoscope or catheter, and internal leakage of a colostomy site. In most cases of perforation of a hollow viscus, mixed bacteria are isolated from the infection; the most common agents include Gram-negative bacilli like E. coli and anaerobic bacteria. Fecal peritonitis results from the presence of feces in the peritoneal cavity. It can result from abdominal trauma and occurs if the large bowel is perforated during surgery.

Disruption of the peritoneum, even in the absence of perforation of a hollow viscus, may also cause infection simply by letting micro- organisms into the peritoneal cavity. Examples include trauma, surgical wound, continuous ambulatory peritoneal dialysis, and intra-peritoneal chemotherapy. Again, in most cases, mixed bacteria are isolated; the most common agents include cutaneous species such as Staphylococcus aureus and coagulase-negative staphylococci, but many others are possible, including fungi such as Candida.

Spontaneous bacterial peritonitis (SBP) is a peculiar form of peritonitis occurring in the absence of an obvious source of contamination. It occurs in patients with excess fluid in their abdomens, particularly in children. Intra-peritoneal dialysis predisposes a patient to peritoneal infection. Systemic infections such as tuberculosis may rarely have a peritoneal localization.

Sterile abdominal surgery, under normal circumstances, causes localized or minimal generalized peritonitis. However, peritonitis may also be caused by the rare case of a sterile foreign body inadvertently left in the abdomen after surgery (e.g., gauze, sponge). Much rarer non-infectious causes may include familial Mediterranean fever, porphyria, and systemic lupus erythematosus.

Treatment

Depending on the severity of the patient’s state, the management of peritonitis may include supportive measures, antibiotics, or surgery. General supportive measures include vigorous intravenous rehydration and correction of electrolyte disturbances. Antibiotics are usually administered intravenously, but they may also be infused directly into the peritoneum. The empiric choice of broad-spectrum antibiotics often consist of multiple drugs, and should be targeted against the most likely agents, depending on the cause of peritonitis; once one or more agents are actually isolated, therapy will of course be targeted on them. Surgery is needed to perform a full exploration and lavage of the peritoneum, as well as to correct any gross anatomical damage that may have caused peritonitis. The exception is spontaneous bacterial peritonitis, which does not always benefit from surgery and may be treated with antibiotics in the first instance.

If properly treated, typical cases of surgically correctable peritonitis (e.g., perforated peptic ulcer, appendicitis, and diverticulitis) have a mortality rate of <10% in otherwise healthy patients, which rises to about 40% in the elderly, and/or in those with significant underlying illness, as well as in cases that present late (after 48 hours). If untreated, generalized peritonitis is almost always fatal.

Mumps

Mumps was a common childhood viral disease, but widespread vaccination has now made it rare in developed countries.

Learning Objectives

Analyze the cause, symptoms, and prevention of mumps

Key Takeaways

Key Points

  • Mumps is a contagious disease that is spread from person to person through contact with respiratory secretions, such as saliva from an infected person. The common symptoms of mumps include inflammation of the salivary glands, pancreas, and testicles; fever; and headache.
  • A physical examination confirms the presence of the swollen glands. Usually, the disease is diagnosed on clinical grounds and no confirmatory laboratory testing is needed.
  • The most common preventative measure against mumps is a vaccination with a mumps vaccine. The vaccine may be given separately or as part of the routine MMR immunization vaccine which also protects against measles and rubella.
  • Like many other viral illnesses, there is no specific treatment for mumps, other than supportive treatment. Death from mumps is very unusual. The disease is self-limiting, and general outcome is good. Known rare complications of mumps include infertility in men and profound hearing loss.

Key Terms

  • orchitis: A painful inflammation of one or both testes.
  • salivary gland: Any of several exocrine glands that produce saliva to break down carbohydrates in food enzymatically.
  • prodromal symptoms: A prodrome is an early symptom (or set of symptoms) that might indicate the start of a disease before specific symptoms occur.
  • parotid gland: Either of a pair of salivary glands located in front of, and below each ear in humans.

Mumps, also known as epidemic parotitis, was a common childhood viral disease caused by the mumps virus. Before the development of vaccination and the introduction of a vaccine in 1949, it was common worldwide, but now, outbreaks are largely confined to developed countries.

Symptoms

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Child with mumps: This child with mumps displays the typical swelling of the salivary glands caused by the mumps virus.

The common symptoms of mumps include inflammation of the salivary glands, pancreas, and testicles; fever, and headache. Swelling of the salivary glands, specifically the parotid gland, is known as parotitis, and it occurs in 60–70% of infections and 95% of patients with symptoms. Parotitis causes swelling and local pain, particularly when chewing. It can occur on one side but is more common on both sides in about 90% of cases. Painful inflammation of the testicles in mumps in known as orchitis. Other symptoms of mumps can include dry mouth, sore face and/or ears and occasionally, in more serious cases, loss of voice. In addition, up to 20% of persons infected with the mumps virus do not show symptoms, so it is possible to be infected and spread the virus without knowing it. Fever and headache are prodromal symptoms of mumps, together with malaise and loss of appetite.

Causes

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Mumps virus: This transmission electron micrograph (TEM) shows the ultrastructure of the mumps virus. It is a roughly spherical particle made up of layers of fatty lipids, large protein molecules, and nucleic acids. The virus is dotted with large protein “spikes” that enable it to gain entry to host cells. Inside lies a core of a single, long molecule of RNA wrapped up in protein that is released into the host cell.

Mumps is a contagious disease that is spread from person to person through contact with respiratory secretions, such as saliva from an infected person. When an infected person coughs or sneezes, the droplets aerosolize and can enter the eyes, nose, or mouth of another person. Mumps can also be spread by sharing food and drinks. The virus can survive on surfaces and then be spread after contact in a similar manner. A person infected with mumps is contagious from approximately six days before the onset of symptoms until about nine days after symptoms start. The incubation period can be anywhere from 14–25 days, but is more typically 16–18 days.

Diagnostics

A physical examination confirms the presence of the swollen glands. Usually, the disease is diagnosed on clinical grounds, and no confirmatory laboratory testing is needed. If there is uncertainty about the diagnosis, a test of saliva or blood may be carried out. An estimated 20–30% of cases are asymptomatic. As with any inflammation of the salivary glands, the level of amylase in the blood is often elevated.

Prevention

The most common preventative measure against mumps is a vaccination with a mumps vaccine. The vaccine may be given separately or as part of the routine MMR immunization vaccine which also protects against measles and rubella. The MMR vaccine is given at ages 12–15 months and then again at four to six years.

Treatment and Complications

Like many other viral illnesses, there is no specific treatment for mumps. Symptoms may be relieved by the application of intermittent ice or heat to the affected neck/testicular area and by the acetaminophen or ibuprofen for pain relief. Warm salt water gargles, soft foods, and extra fluids may also help relieve symptoms. Patients are advised to avoid acidic foods and beverages, since these stimulate the salivary glands, which can be painful.

Death from mumps is very unusual. The disease is self-limiting, and general outcome is good, even if other organs are involved. Known complications of mumps include:

  • In teenage males and men, complications from orchitis such as infertility or sub-fertility are rare, but present.
  • Spontaneous abortion in about 27% of cases during the first trimester of pregnancy.
  • Mild forms of meningitis in up to 10% of cases.
  • Profound hearing loss is very rare, but mumps was the leading cause of acquired deafness before the advent of the mumps vaccine.

After the illness, life-long immunity to mumps generally occurs; re-infection is possible but tends to be mild and atypical.

Lactose Intolerance

Lactose intolerance is the inability to digest lactose, a sugar found in milk, due to a lack of the enzyme lactase.

Learning Objectives

Analyze lactose intolerance and tolerance

Key Takeaways

Key Points

  • Symptoms of lactose intolerance include abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi (rumbling stomach), and/or vomiting after consuming significant amounts of lactose. Individuals may be lactose intolerant to varying degrees, depending on the severity of these symptoms.
  • Most mammals normally become lactose intolerant after weaning, but some human populations have developed lactase persistence, in which lactase production continues into adulthood. These populations (northern Europe, India, and a few groups in Africa) are dairying cultures.
  • Lactase deficiency has a number of causes, and is therefore classified as one of three types: primary, secondary, or congenital. Primary lactase deficiency is genetic and normal as most adults worldwide do not maintain lactase production.
  • Secondary/acquired/transient lactase deficiency is caused by an injury to the small intestine. Congenital lactase deficiency prevents lactase expression from birth, making nourishment from breast milk impossible.
  • Lactose intolerance is not an allergy, because it is not an immune response, but rather a problem with digestion caused by lactase deficiency. Milk allergy is a separate condition, with distinct symptoms that occur when the presence of milk proteins trigger an immune reaction.
  • Primary lactase deficiency is genetic, secondary/acquired/transient lactase deficiency is caused by an injury to the small intestine, and congenital lactase deficiency prevents lactase expression from birth.

Key Terms

  • lactose: The disaccharide sugar of milk and dairy products, C12H22O11, (a product of glucose and galactose) used as a food and in medicinal compounds.
  • lactose intolerance: The inability to fully metabolize lactose.
  • lactase: A β-galactosidase enzyme that is involved in the hydrolysis of the disaccharide lactose into constituent galactose and glucose monomers.

Examples

Those who are lactose intolerant can be more tolerant of traditionally made yogurt than of milk because it contains lactase produced by the bacterial cultures used to make the yogurt. Frozen yogurt, if cultured similarly to its unfrozen counterpart, will contain similarly reduced lactose levels. However, many commercial brands contain milk solids, increasing the lactose content.

Lactose intolerance, also called lactase deficiency and hypolactasia, is the inability to digest lactose, a sugar found in milk and, to a lesser extent, in milk-derived dairy products. Lactose intolerant individuals have insufficient levels of lactase, the enzyme that metabolizes lactose into glucose and galactose, in their digestive system. In most cases, this causes symptoms such as abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi (rumbling stomach), and/or vomiting after consuming significant amounts of lactose. Some studies in the U.S. and elsewhere suggest that milk consumption by lactose intolerant individuals may be a significant cause of irritable bowel syndrome.

This image shows a lactose molecule.

Lactose: Lactose, a disaccharide of β-D-galactose and β-D-glucose, is normally broken down by the enzyme lactase into its component monosaccharides. Individuals who suffer from lactose intolerance have insufficient levels of lactase to break down the lactose in milk and dairy products.

Most mammals normally become lactose intolerant after weaning, but some human populations have developed lactase persistence, in which lactase production continues into adulthood. It is estimated that 75% of adults worldwide show some decrease in lactase activity during adulthood. The frequency of decreased lactase activity ranges from 5% in northern Europe through 71% for Sicily to more than 90% in some African and Asian countries. This distribution is now thought to have been caused by recent natural selection favoring lactase persistent individuals in cultures that rely on dairy products. While it was first thought that this would mean that populations in Europe, India, and Africa that had high frequencies of lactase persistence shared a single mutation, it has now been shown that lactase persistence is caused by several independently occurring mutations.

Causes

Primary lactase deficiency is genetic, only affects adults, and is caused by the absence of a lactase persistence allele. It is the most common cause of lactose intolerance as a majority of the world’s population lacks these alleles. Secondary, acquired, or transient lactase deficiency is caused by an injury to the small intestine, usually during infancy, from acute gastroenteritis, diarrhea, chemotherapy, intestinal parasites, or other environmental causes. Congenital lactase deficiency is a very rare, autosomal recessive genetic disorder that prevents lactase expression from birth. It is particularly common in Finland. People with congenital lactase deficiency who are unable to digest lactose from birth are unable to digest breast milk.

Effects on Nutrition

While dairy products can be a significant source of nutrients in some societies, there is no evidence that lactose intolerance has any adverse impact on nutrition where consumption is the norm among adults. Congenital lactase deficiency (CLD), where the production of lactase is inhibited from birth, can be dangerous in any society because of infants’ nutritional reliance on breast milk during their first months. Before the 20th century, babies born with CLD were not expected to survive, but these death rates can now be lowered using soybean-derived infant formulas and manufactured lactose-free dairy products. Beyond infancy, individuals affected by CLD usually have the same nutritional concerns as any lactose-intolerant adult.

Lactose cannot be directly absorbed through the wall of the small intestine into the bloodstream so, in the absence of lactase, it passes intact into the colon. Bacteria in the colon are able to metabolize lactose and the resulting fermentation produces copious amounts of gas (a mixture of hydrogen, carbon dioxide, and methane) that causes the various abdominal symptoms. The unabsorbed sugars and fermentation products also raise the osmotic pressure of the colon, resulting in an increased flow of water into the bowels (diarrhea).

Assessment and Treatment of Lactose Intolerance

To assess lactose intolerance, intestinal function is challenged by ingesting more dairy products than can be readily digested. Clinical symptoms typically appear within 30 minutes, but may take up to two hours, depending on other foods and activities. Substantial variability in response (symptoms of nausea, cramping, bloating, diarrhea, and flatulence) is to be expected, as the extent and severity of lactose intolerance varies among individuals.

It is important to distinguish lactose intolerance from milk allergy, an abnormal immune response (usually) to milk proteins. This may be done in diagnosis by giving lactose-free milk, producing no symptoms in the case of lactose intolerance, but the same reaction as to normal milk if it is a milk allergy. An intermediate result might suggest that the person has both conditions. Since lactose intolerance is the normal state for most adults worldwide, it is not considered a disease and a medical diagnosis is not normally required, although tests are available if confirmation is necessary.

Lactose intolerance is not considered a condition that requires treatment in societies where the diet contains relatively little dairy. However, those living among societies that are largely lactose-tolerant may find lactose intolerance troublesome. Although there are still no methodologies to reinstate lactase production, some individuals have reported that their intolerance varies over time, depending on health status and pregnancy. About 44% of lactose intolerant women regain the ability to digest lactose during pregnancy. This might be caused by slow intestinal transit and intestinal flora changes during pregnancy.

Peptic Ulcer Disease

A peptic ulcer, also known as peptic ulcer disease, is an erosion in the wall of the stomach, duodenum, or esophagus.

Learning Objectives

List the causes of and treatments for peptic ulcer disease

Key Takeaways

Key Points

  • 70–90% of peptic ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach.
  • Diagnosis is mainly established based on the characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer.
  • Treatment of H. pylori usually leads to clearing of infection, relief of symptoms, and eventual healing of ulcers.
  • Gas in the peritoneal cavity, shown on an erect chest x-ray or supine lateral abdominal x-ray, is an omen of perforated peptic ulcer disease, which requires emergency surgery.
  • Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery.
  • Most bleeding ulcers require endoscopy urgently to stop bleeding with cautery, injection, or clipping.
  • During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue.
  • A gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and muscularis propria, produced by acid-pepsin aggression.
  • Ulcers are not purely an infectious disease and that psychological factors do play a significant role.
  • Diagnosis is mainly established based on the characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer.
  • Gastric ulcers are most often localized on the lesser curvature of the stomach.
  • Gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.
  • Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery.
  • Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours commonly accompanies ulcers.
  • Typical ulcers tend to heal and recur and as a result the pain may occur for few days and weeks and then wane or disappear.

Key Terms

  • prostaglandin: Any of a group of naturally occurring lipids derived from the C20 acid prostanoic acid; they have a number of physiological functions and may be considered to be hormones.
  • NSAID: Any drug of the non-steroidal anti-inflammatory class used as a pain reliever.
  • gastrin: A hormone that stimulates the production of gastric acid in the stomach.
  • gastritis: Inflammation of the lining of the stomach, characterized by nausea, loss of appetite, and upper abdominal discomfort or pain.

A peptic ulcer, also known as peptic ulcer disease, is an erosion in the wall of the stomach, duodenum, or esophagus. As many as 70–90% of such ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach. Ulcers can also be caused or worsened by drugs such as aspirin, ibuprofen, and other NSAIDs.

Symptoms

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Deep gastric ulcer: This image, acquired via endoscope, shows a deep gastric ulcer.

Symptoms of a peptic ulcer include abdominal pain, classically near the stomach with severity relating to mealtimes, about three hours after eating a meal; bloating and abdominal fullness; nausea; copious vomiting; loss of appetite and weight loss; vomiting of blood; and melena, which are tarry, foul-smelling feces due to oxidized iron from hemoglobin. Rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis. This is extremely serious and requires immediate surgery.

Causes

A major causative factor of ulcers is chronic inflammation due to Helicobacter pylori that colonizes the mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis, resulting in a defect in the regulation of gastrin production by that part of the stomach. Gastrin secretion can either be increased, or as in most cases, decreased, resulting in a too basic or too acidic stomach environment, respectively. A decrease in acid can promote H. pylori growth and an increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation.

Another major cause is the use of NSAIDs. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins.

Researchers also continue to look at stress as a possible cause, or at least complication, in the development of ulcers. There is debate as to whether psychological stress can influence the development of peptic ulcers. Burns and head trauma, however, can lead to physiologic stress ulcers, which are reported in many patients who are on mechanical ventilation.

Diagnosis

The diagnosis is mainly established based on the characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer. In some cases, doctors may treat ulcers without diagnosing them with specific tests and observe whether the symptoms resolve, this indicating that their primary diagnosis was accurate.

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Gastric ulcer: This endoscopic image shows a gastric ulcer, which upon biopsy was shown to be gastric cancer.

Confirmation of the diagnosis is made with the help of tests such as endoscopies or barium contrast x-rays. The tests are typically ordered if the symptoms do not resolve after a few weeks of treatment. Tests are also given when first appear in a person who is over age 45 or who has other symptoms such as weight loss, because stomach cancer can cause similar symptoms. Also, when severe ulcers resist treatment, particularly if a person has several ulcers or the ulcers are in unusual places, a doctor may suspect an underlying condition that causes the stomach to overproduce acid.

An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.

If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to “free gas” within the peritoneal cavity. If the patient stands erect, as when having a chest x-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest x-ray or supine lateral abdominal x-ray, is an omen of perforated peptic ulcer disease.

Treatment

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Benign gastric ulcer: This gastric ulcer was found in tissue removed during a gastrectomy.

Younger patients with ulcer-like symptoms are often treated with antacids. The ability of antacids to neutralize acidity by increasing the pH or blocking the secretion of acid by gastric cells is critical in reducing acidity in the stomach. Patients who are taking NSAIDs may also be prescribed a prostaglandin analogue in order to help prevent peptic ulcers by replacing the prostaglandins whose formation is blocked by NSAID use.

When H. pylori infection is present, the most effective treatments are combinations of two antibiotics, such as Clarithromycin, Amoxicillin, Tetracycline, and Metronidazole; and one proton pump inhibitor, sometimes in combination with antacids. In complicated, treatment-resistant cases, three antibiotics may be used together with a proton pump inhibitor. Treatment of H. pylori usually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics.

Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation. Most bleeding ulcers require endoscopy urgently to stop bleeding with cautery, injection, or clipping.