GI Flashcards
(6 cards)
Ulcerative Colitis
Ulcerative colitis may start at any age but usually begins before age 30, usually between the ages of 14 and 24. A small group of people have their first attack between the ages of 50 and 70.
Ulcerative colitis usually starts in the rectum (ulcerative proctitis). It may stay confined to the rectum or over time extend to involve the entire colon. In some people, most of the large intestine is affected at once.
Ulcerative colitis usually does not affect the full thickness of the wall of the large intestine and hardly ever affects the small intestine. The affected parts of the intestine have shallow ulcers (sores). Unlike Crohn disease, ulcerative colitis does not cause fistulas or abscesses.
The cause of ulcerative colitis is not known for certain, but heredity and an overactive immune response in the intestine seem to be contributing factors. Cigarette smoking, which seems to contribute to the development and periodic flare-ups of Crohn disease, seems to decrease the risk of ulcerative colitis. However, smoking in order to reduce the risk of ulcerative colitis is ill-advised in light of the many health problems that smoking can cause. Some evidence suggests that isotretinoin, which is a drug used to treat acne, can increase the risk of ulcerative colitis.
Symptoms
The symptoms of ulcerative colitis occur in flare-ups. A flare-up may be sudden and severe, causing violent diarrhea that typically contains mucus and blood, high fever, abdominal pain, and peritonitis (inflammation of the lining of the abdominal cavity). During such flare-ups, the person is profoundly ill. More often, a flare-up begins gradually, and the person has an urgency to have a bowel movement (defecate), mild cramps in the lower abdomen, and visible blood and mucus in the stool. A flare-up can last days or weeks and can recur at any time.
When the disease is limited to the rectum and the sigmoid colon, the stool may be normal or hard and dry. However, mucus containing large numbers of red and white blood cells is discharged from the rectum during or between bowel movements. People may or may not have mild general symptoms of illness, such as fever.
If the disease extends farther up the large intestine, the stool is looser, and the person may have more than 10 bowel movements a day. Often, the person has severe abdominal cramps and distressing, painful spasms that accompany the urge to defecate. There is no relief at night. The stool may be watery or contain pus, blood, and mucus. Frequently, the stool consists almost entirely of blood and pus. The person also may have a fever and a poor appetite and may lose weight.
Complications
Bleeding, the most common complication, often causes iron deficiency anemia. In nearly 10% of people with ulcerative colitis, a rapidly progressive first attack becomes very severe, with massive bleeding, perforation, or widespread infection.
Toxic colitis, a particularly severe complication, involves damage to the entire thickness of the intestinal wall. The damage to the nerves and muscles of the bowel wall causes ileus—a condition in which the normal contractile movements of the intestinal wall temporarily stop—and thus the intestinal contents are not propelled along their way. Abdominal expansion (distention) develops. As toxic colitis worsens, the large intestine loses muscle tone and within days—or even hours—it starts to expand. This complication may cause a high fever and abdominal pain. Sometimes there is a perforation of the large intestine and the person develops peritonitis. X-rays of the abdomen may show expansion of the bowel and the presence of gas inside the wall of the paralyzed sections of intestine.
Colon cancer starts to become more common about 7 years from when the illness started in people with extensive colitis. The risk of colon cancer is highest when the entire large intestine is affected and increases the longer the person has had ulcerative colitis. After 25 years of disease, about 9% of people will have developed cancer, and cancer is found each year thereafter in about 1 of 100 to 200 people. Colonoscopy (examination of the large intestine using a flexible viewing tube) every 1 to 2 years is advised for people who have had ulcerative colitis for more than 8 to 10 years. During colonoscopy, tissue samples (biopsies) are obtained from areas throughout the large intestine for microscopic examination to detect the early warning signs of cancer (dysplasia).
Other complications can occur, as in Crohn disease. When ulcerative colitis causes a flare-up of gastrointestinal symptoms, the person also may have inflammation of the joints (arthritis), inflammation of the whites of the eyes (episcleritis), inflamed skin nodules (erythema nodosum), and blue-red skin sores containing pus (pyoderma gangrenosum). When ulcerative colitis is not causing a flare-up of gastrointestinal symptoms, the person still may have pyoderma gangrenosum about half of the time, whereas inflammation of the spine (ankylosing spondylitis), inflammation of the pelvic joints (sacroiliitis), and inflammation of the inside of the eye (uveitis) are liable to occur entirely without relation to the bowel disease. Rarely, blood clots develop in the veins.
Although people with ulcerative colitis commonly have minor liver dysfunction, only about 1 to 3% have symptoms of mild to severe liver disease. Severe liver disease can include inflammation of the liver (chronic active hepatitis); inflammation of the bile ducts (primary sclerosing cholangitis), which narrow and eventually close; and replacement of functional liver tissue with scar tissue (cirrhosis). Inflammation of the bile ducts may appear many years before any intestinal symptoms of ulcerative colitis. The inflammation greatly increases the risk of cancer of the bile ducts and also seems to be associated with a sharp increase in the risk of colon cancer.
Diagnosis
Doctors suspect ulcerative colitis in a person with recurring bloody diarrhea accompanied by cramps and a strong urge to defecate, particularly if the person has other complications, such as arthritis or liver problems, and a history of similar attacks.
Doctors examine the stool to look for parasites and rule out bacterial infections.
A sigmoidoscopy (an examination of the sigmoid colon using a flexible viewing tube) confirms the diagnosis and permits a doctor to directly observe the severity of the inflammation, take samples of mucus or stool for culture, and remove tissue samples of affected areas. Even during symptom-free intervals, the intestine rarely appears entirely normal, and tissue samples removed for microscopic examination usually show chronic inflammation. A colonoscopy is usually not necessary, but doctors may need to do a colonoscopy if the inflammation extends beyond the reach of the sigmoidoscope.
Blood tests do not confirm the diagnosis but may reveal that the person has anemia, increased numbers of white blood cells, a low level of the protein albumin, and an elevated erythrocyte sedimentation rate (ESR) or C-reactive protein level, which indicate active inflammation.
Barium enema x-rays of the abdomen may indicate the severity and extent of the disease but are not done when the disease is active, such as during a flare-up.
Recurring or severe symptoms
Doctors examine people when their typical symptoms return but they do not always do tests. If symptoms have been more frequent or longer-lasting than usual, doctors may do sigmoidoscopy or colonoscopy and a blood count. When symptoms are severe, doctors may take x-rays to look for a dilated or perforated intestine.
Prognosis
Ulcerative colitis is usually chronic, with repeated flare-ups and remissions (periods of no symptoms). In about 10% of people, an initial attack progresses rapidly and results in serious complications. Another 10% recover completely after a single attack. The remaining people have some degree of recurring disease.
Complete removal of the large intestine and rectum (proctocolectomy) cures ulcerative colitis. The risk of colon cancer is eliminated, life expectancy is restored to normal, and quality of life improves.
People who have ulcerative proctitis have the best prognosis. Severe complications are unlikely. However, in about 20 to 30% of people, the disease eventually spreads to the large intestine (thus evolving into ulcerative colitis). In people who have proctitis that has not spread, surgery is rarely required, cancer rates are not increased, and life expectancy is normal.
Colon cancer
The long-term survival rate for people with colon cancer caused by ulcerative colitis is about 50%. Most people survive if the diagnosis is made during the early stages and the colon is removed in time.
Treatment
Treatment aims to control the inflammation, reduce symptoms, and replace any lost fluids and nutrients.
Iron supplements may offset anemia caused by ongoing blood loss in the stool. Raw fruits and vegetables should be avoided to reduce injury to the inflamed lining of the large intestine. A diet free of dairy products may decrease symptoms and is worth trying but need not be continued if no benefit is noted. Doctors give calcium and vitamin D supplements if people maintain a dairy-free diet.
Small doses of loperamide are taken for relatively mild diarrhea. For more intense diarrhea, higher doses of loperamide may be needed. In severe cases, however, a doctor must closely monitor the person taking these antidiarrheal drugs to avoid suddenly causing toxic colitis.
Specific treatment depends on the severity of people’s symptoms.
Anti-inflammatory drugs
Drugs such as sulfasalazine, olsalazine, mesalamine, and balsalazide are used to reduce the inflammation of ulcerative colitis and to prevent flare-ups of symptoms.
Crohn’s Disease
Crohn disease (regional enteritis, granulomatous ileitis, or ileocolitis) is chronic inflammation of the intestinal wall that typically involves the lower part of the small intestine, the upper part of the large intestine, or both but may affect any part of the digestive tract.
In the past few decades, Crohn disease has become more common worldwide. However, it is most common among people of Northern European and Anglo-Saxon descent. It occurs about equally in both sexes, often runs in families, and seems to be more common among Ashkenazi Jews. Most people develop Crohn disease before age 30, usually between the ages of 14 and 24.
Most commonly, Crohn disease occurs in the last portion of the small intestine (ileum) and in the large intestine, but it can occur in any part of the digestive tract, from the mouth to the anus and even in the skin around the anus. Crohn disease affects the small intestine alone (35% of people), the large intestine alone (20% of people), or both the last portion of the small intestine and the large intestine (45% of people). The rectum is rarely affected, unlike in ulcerative colitis, in which the rectum is always involved. However, infections and other complications around the anus are not unusual. The disease may affect some segments of the intestinal tract while leaving normal segments (called skip areas) between the affected areas. Where Crohn disease is active, the full thickness of the bowel is usually involved.
The cause of Crohn disease is not known for certain, but many researchers believe that a dysfunction of the immune system causes the intestine to overreact to an environmental, dietary, or infectious agent. Certain people may have a hereditary predisposition to this immune system dysfunction. Cigarette smoking seems to contribute to both the development and the periodic flare-ups (bouts or attacks) of Crohn disease. Oral contraceptives may increase the risk of Crohn disease.
Symptoms
The most common early symptoms of Crohn disease are chronic diarrhea (which sometimes is bloody when the large intestine is severely affected), crampy abdominal pain, fever, loss of appetite, and weight loss. Symptoms may continue for days or weeks and may resolve without treatment. Complete and permanent recovery after a single attack is extremely rare. Crohn disease almost always flares up at irregular intervals throughout a person’s life. Flare-ups can be mild or severe, brief or prolonged. Severe flare-ups can lead to intense, constant pain, fever, and dehydration. Why the symptoms come and go and what triggers new flare-ups or determines their severity is not known. Recurrent inflammation tends to appear in the same area of the intestine, but it may spread to adjacent areas after a diseased segment has been removed surgically.
In children, abdominal pain and diarrhea often are not the main symptoms and may not appear at all. Instead, the main symptoms may be slow growth, joint inflammation, fever, or weakness and fatigue resulting from anemia.
Complications
Common complications of inflammation include
Intestinal blockage (obstruction)
Abscesses (pus-filled pockets of infection) in the abdomen
Fistulas (abnormal connecting channels between the intestine and skin or other organs)
Anal fissures (tears in the skin of the anus), abscesses, and fistulas
Scarring due to chronic inflammation can cause intestinal blockage. Deep ulcers that penetrate through the bowel wall can create abscesses or open fistulas. Fistulas may connect two different parts of the intestine. Fistulas also may connect the intestine and bladder or the intestine and the skin surface, especially around the anus. Although fistulas from the small intestine are common, wide-open holes (perforations) are rare. Fissures in the skin of the anus are common.
When the large intestine is affected extensively by Crohn disease, rectal bleeding commonly occurs. After many years, the risk of colon cancer (cancer of the large intestine) is greatly increased. About one third of people who develop Crohn disease have problems around the anus, especially fistulas and fissures in the lining of the mucus membrane of the anus.
Crohn disease may lead to complications in other parts of the body. These complications include gallstones, inadequate absorption of nutrients, urinary tract infections, kidney stones, and deposits of the protein amyloid in several organs (amyloidosis).
When Crohn disease causes a flare-up of gastrointestinal symptoms, the person may also have inflammation of the joints (arthritis), inflammation of the whites of the eyes (episcleritis), mouth sores (aphthous stomatitis), inflamed skin nodules on the arms and legs (erythema nodosum), and blue-red skin sores containing pus (pyoderma gangrenosum). Even when Crohn disease is not causing a flare-up of gastrointestinal symptoms, the person still may have inflammation of the spine (ankylosing spondylitis), inflammation of the pelvic joints (sacroiliitis), inflammation inside the eye (uveitis), or inflammation of the bile ducts (primary sclerosing cholangitis) entirely without relation to the bowel disease.
Diagnosis
A doctor may suspect Crohn disease in a person with recurring crampy abdominal pain and diarrhea, particularly if the person has a family history of Crohn disease or a history of problems around the anus. Other clues to the diagnosis may include inflammation in the joints, eyes, or skin or, in a child, stunted growth. The doctor may feel a lump or fullness in the lower part of the abdomen, most often on the right side.
No laboratory test specifically identifies Crohn disease, but blood tests may show anemia, abnormally high numbers of white blood cells, low levels of the protein albumin, and other indications of inflammation such as an elevated erythrocyte sedimentation rate or level of C-reactive protein.
People who have severe abdominal pain and tenderness have a computed tomography (CT) scan of their abdomen. CT may show a blockage, abscesses or fistulas, and other possible causes of inflammation of the abdomen (such as appendicitis).
People who have less severe inflammation or who have had symptoms that recur over a period of time have CT or magnetic resonance enterography, or plain x-rays are taken after barium is swallowed or given by enema. Another way in which the small intestine can be evaluated is with wireless capsule endoscopy (see page Video Capsule Endoscopy).
People who have little pain and mostly diarrhea undergo a colonoscopy (an examination of the large intestine with a flexible viewing tube) and a biopsy (removal of a tissue specimen for microscopic examination). If Crohn disease is limited to the small intestine, colonoscopy will not detect the disease unless the colonoscope is advanced all the way through the colon into the last part of the small intestine where the inflammation most often resides.
Prognosis
Crohn disease has no known cure and is characterized by intermittent flare-ups of symptoms. Flare-ups may be mild or severe, few or frequent.
Crohn disease usually does not shorten a person’s life. However, some people die of cancer of the digestive tract, which may develop more frequently than normally expected in long-standing Crohn disease.
Treatment
Many treatments help reduce inflammation and relieve symptoms.
Antidiarrheal drugs
These drugs, which may relieve cramps and diarrhea (see Agents Used to Prevent or Treat Constipation), include drugs that have anticholinergic effects (drugs that block certain pathways of the nervous system―see page Anticholinergic: What Does It Mean?) such as diphenoxylate, loperamide, deodorized opium tincture, and codeine. They are taken by mouth—preferably before meals. Taking methylcellulose or psyllium preparations sometimes helps prevent anal irritation by making the stool firmer.
Anti-inflammatory drugs
Sulfasalazine and related drugs such as mesalamine, olsalazine, and balsalazide reduce inflammation. These drugs can suppress symptoms when they occur and reduce inflammation, especially in the large intestine. Typically these drugs are taken by mouth. Mesalamine is also available as a suppository or enema. Mesalamine may be effective in preventing recurrences. These drugs do not work as well for relieving severe flare-ups.
Corticosteroids such as prednisone, which is given by mouth, may dramatically reduce fever and diarrhea, relieve abdominal pain and tenderness, and improve appetite and sense of well-being. However, long-term corticosteroid therapy invariably results in side effects
Diseases of Oesohagus
GERD
Achalasia
Tumours
In gastroesophageal reflux (gastroesophageal reflux disease), stomach acid and enzymes flow backward from the stomach into the esophagus, causing inflammation and pain in the esophagus.
Reflux occurs when the ring-shaped muscle that normally prevents the contents of the stomach from flowing back into the esophagus (lower esophageal sphincter) does not function properly.
The most typical symptom is heartburn (a burning pain behind the breastbone).
The diagnosis is based on symptoms.
Treatment is avoiding trigger substances (such as alcohol and fatty foods) and taking drugs that reduce stomach acid.
Gastroesophageal reflux disease (GERD) is common. It occurs in 10 to 20% of adults. It also occurs frequently in infants, typically beginning at birth.
Acid and enzymes reflux when the lower esophageal sphincter, the ring-shaped muscle that normally prevents the contents of the stomach from flowing back into the esophagus, is not functioning properly. When a person is standing or sitting, gravity helps to prevent the reflux of stomach contents into the esophagus, which explains why reflux can worsen when a person is lying down. Reflux is also more likely to occur soon after meals, when the volume and acidity of contents in the stomach are higher and the sphincter is less likely to work properly. Factors contributing to reflux include weight gain, fatty foods, caffeinated and carbonated beverages, alcohol, tobacco smoking, and certain drugs. Types of drugs that interfere with lower esophageal sphincter function include those that have anticholinergic effects (such as many antihistamines and some antidepressants), calcium channel blockers, progesterone, and nitrates. Alcohol and coffee also contribute by stimulating acid production. Delayed emptying of the stomach (for example, due to diabetes or use of opioids) can also worsen reflux.
Symptoms Heartburn (a burning pain behind the breastbone) is the most obvious symptom of gastroesophageal reflux. Heartburn may be accompanied by regurgitation, in which the stomach contents reach the mouth. If stomach contents reach the mouth, they sometimes cause sore throat, hoarseness, cough, or a sensation of a lump in the throat (globus sensation). Sometimes, stomach contents trickle into the lungs, causing cough and/or wheezing.
Inflammation of the esophagus (esophagitis) may cause pain with swallowing (odynophagia). Some people have bleeding that is usually slight but can be massive. The blood may be vomited up or may pass through the digestive tract, resulting in the passage of dark, tarry stools (melena) or bright red blood, if the bleeding is heavy enough.
Esophageal ulcers are open sores on the lining of the esophagus. They can cause chest pain that is usually located behind the breastbone or just below it, similar to the location of heartburn.
Narrowing (stricture) of the esophagus caused by reflux makes swallowing solid foods increasingly more difficult.
Prolonged irritation causes the cells lining the esophagus to change, which results in a condition called Barrett esophagus. Changes may occur even without symptoms. These abnormal cells are precancerous and progress to cancer in some people.
Treatment
Proton pump inhibitors, the most powerful drugs for reducing stomach acid production, are usually the most effective treatment for gastroesophageal reflux. Healing typically requires taking the drugs for a 4- to 12-week period. These drugs may be continued long-term, but if this is necessary, doctors try to use a lower dose. Alternatives to proton pump inhibitors include histamine-2 (H2) blockers and drugs that stimulate the movement of contents through the esophagus, stomach, and intestines (called promotility drugs). However, these drugs are not as effective as proton pump inhibitors.
Esophageal narrowing is treated by repeatedly dilating the narrowed area using balloons. If dilation is successful, narrowing does not seriously limit what a person can eat.
Achalasia
A disorder in which the rhythmic contractions of the esophagus are absent, the lower esophageal sphincter does not relax normally, and the resting pressure of the lower esophageal sphincter is increased.
Achalasia results from a malfunction of the nerves controlling the rhythmic contractions of the esophagus. The cause of the nerve malfunction is not known, but viral and autoimmune causes are suspected. Certain tumors may cause achalasia either by directly narrowing (constricting) the lower esophageal sphincter or by infiltrating the nerves of the esophagus. Chagas disease, which causes the destruction of clusters of nerve cells (autonomic ganglia), may also result in achalasia.
Symptoms
The tight lower esophageal sphincter causes the part of the esophagus above it to enlarge greatly. This enlargement contributes to many of the symptoms. Difficulty swallowing (dysphagia) both solids and liquids is the main symptom. Although less common, chest pain may occur during swallowing or for no apparent reason. About one third of people who have achalasia regurgitate undigested food while sleeping. They may inhale food into their lungs, which can cause coughing, a lung abscess, infection of the airways, bronchiectasis, or aspiration pneumonia. Undigested food typically remains in the esophagus. Mild to moderate weight loss also occurs.
Treatment
No treatment restores peristalsis. The aim of treatment is to relieve symptoms by decreasing pressure in the lower esophageal sphincter.
The first treatment is to dilate the sphincter mechanically by inflating a large balloon inside it. This procedure helps about 85% of the time, but repeated dilations may be needed. In fewer than 2% of people with achalasia, the esophagus ruptures during the dilation procedure. Esophageal rupture leads to severe inflammation in the chest outside the esophagus (mediastinitis) and, in rare cases, is fatal if not treated appropriately. Immediate surgery is needed to close the rupture in the wall of the esophagus.
Certain drugs can help relax the sphincter. They have limited effectiveness but may prolong the time between dilations. The most common drugs are nitrates (for example, isosorbide dinitrate placed under the tongue before meals) or calcium channel blockers (for example, nifedipine).
As an alternative to mechanical dilation, a doctor may inject botulinum toxin into the lower esophageal sphincter. This therapy is almost as effective as mechanical dilation with balloons, giving symptom relief for 70 to 80% of people, but the relief may last only 6 months to 1 year.
Tumours
The most common types of esophageal cancer are squamous cell carcinoma and adenocarcinoma, which develop in the cells that line the wall of the esophagus. Squamous cell carcinoma is more common in the upper part of the esophagus. Adenocarcinoma is more common in the lower part. These cancers may appear as a narrowing (stricture) of the esophagus, a lump, an abnormal flat area (plaque), or an abnormal connection (fistula) between the esophagus and the airways that supply the lungs. Less common types of esophageal cancer include leiomyosarcomas (cancers of the smooth muscle of the esophagus) and metastatic cancer (cancer that has spread from elsewhere in the body).
Risk Factors Tobacco use (any kind) and alcohol are the main risk factors for developing esophageal cancer, although more so for squamous cell carcinoma than for adenocarcinoma. People who have had certain human papillomavirus infections, who have had head and neck cancer, or who have undergone radiation therapy to the esophagus for treatment of other nearby cancers are at greater risk of developing esophageal cancer.
People with an existing disorder of the esophagus, such as achalasia, esophageal webs (Plummer-Vinson syndrome), or narrowing due to having once swallowed a corrosive substance (such as lye), are also at greater risk of developing squamous cell esophageal cancer. Most adenocarcinomas develop in people who have a precancerous condition called Barrett esophagus. Barrett esophagus develops from prolonged irritation of the esophagus caused by the repeated backflow of stomach acid ( gastroesophageal reflux). Obese people have an increased risk of adenocarcinoma because of their higher risk of gastroesophageal reflux.
Symptoms
Early-stage esophageal cancer may go unnoticed. The first symptom of esophageal cancer is usually difficulty in swallowing solid foods, which develops as the growing cancer narrows the esophagus. Several weeks later, swallowing soft foods and then liquids and saliva becomes difficult. Weight loss is common, even when the person continues to eat well. People may have chest pain, which feels like it travels to the back.
As the cancer progresses, it commonly invades various nerves and other tissues and organs. The tumor may compress the nerve that controls the vocal cords, which can lead to hoarseness. Compression of surrounding nerves may cause Horner syndrome, spinal pain, and hiccups. The cancer usually spreads to the lungs, where it may cause shortness of breath, and to the liver, where it may cause fever and abdominal swelling. Spread to bones may cause pain. Spread to the brain may cause headache, confusion, and seizures. Spread to the intestines may cause vomiting, blood in the stool, and iron deficiency anemia. Spread to the kidneys often causes no symptoms.
In late stages, the cancer may completely block the esophagus. Swallowing becomes impossible, so secretions build up in the mouth, which can be very distressing.
Diagnosis Endoscopy and biopsy Barium swallow Computed tomography (CT) Ultrasonography
Treatment
Surgical removal
Chemotherapy combined with radiation therapy
Relief of symptoms
Acute and Chronic Gastritis
Gastritis is divided into two categories based on how severe it is:
Erosive
Nonerosive
Erosive gastritis is more severe than nonerosive gastritis. This form involves both inflammation and wearing away (erosion) of the stomach lining. The cells that produce mucus to protect the stomach lining from acid are missing or are damaged. Erosive gastritis typically develops suddenly (called acute erosive gastritis) but may develop slowly (called chronic erosive gastritis), usually in people who are otherwise healthy.
Nonerosive gastritis is characterized by changes in the stomach lining that range from wasting away (atrophy) of the stomach lining to transformation of stomach tissue into another type of intestinal tissue (metaplasia). Often, several types of white blood cells accumulate in the stomach and cause varying degrees of inflammation. The white blood cells may cause inflammation in the entire stomach or only in certain parts.
Causes of Gastritis
The specific types of gastritis are caused by many factors, including infection, stress, injury, certain drugs, and disorders of the immune system.
Erosive gastritis is caused by alcohol; stress; irritants such as drugs, especially aspirin and other nonsteroidal anti-inflammatory drugs ( NSAIDs); Crohn disease; bacterial and viral infections; and the ingestion of corrosive substances. In some people, even a baby aspirin taken daily can injure the stomach lining. Less commonly, radiation, viral infections (such as cytomegalovirus), and direct injuries (such as by the insertion of a nasogastric tube) can cause erosive gastritis.
Nonerosive gastritis can be caused by Helicobacter pylori infection.
Infectious gastritis not caused by Helicobacter pylori is rare.
Bacterial gastritis, which may require emergency surgery and can cause death, occurs mainly after a sudden blockage of blood flow (ischemia) to the stomach, ingestion of corrosive substances, or exposure to radiation.
Viral gastritis or fungal gastritis may develop in people who have had a prolonged illness or an impaired immune system, such as those who have AIDS or cancer or those who take immunosuppressant drugs.
Acute stress gastritis, a form of erosive gastritis, is caused by a sudden illness or injury. The injury may not even be to the stomach. For example, extensive skin burns, head injuries, and injuries involving major bleeding are typical causes. Exactly why serious illness can lead to gastritis is not known but may be related to decreased blood flow to the stomach, an increase in the amount of acid in the stomach, and/or to impairment of the stomach lining’s ability to protect and renew itself.
Acute gastritis
Acute gastritis refers to a transient inflammation of the gastric mucosa. It is most commonly associated with local irritants such as bacterial endotoxins, caffeine, alcohol, and aspirin. The complications of persons with acute gastritis vary. Persons with aspirin -related gastritis can be totally unaware of the condition or may complain only of heartburn or sour stomach. Gastritis associated with excessive alcohol consumption is a different situation; it often causes transient gastric distress, which may lead to vomiting and, in more severe situations, to bleeding and hematemesis. Acute gastritits is usually a self-limiting disorder; complete regeneration usually occurs within several days.
Chronic Gastritis
Chronic gastritis is a separate entity from acute gastritis. It is characterized by the absence of visible erosions and the presence of chronic inflammatory changes leading eventually to atrophy of the glandular epithelium of the stomach. There are two major forms of chronic gastritis: autoimmune gastritis and chronic infectious gastritis.
Peptic Ulcer Disease
Peptic ulcer is a term used to describe a group of ulcerative disorders that occur in areas of the upper gastrointestinal tract that are exposed to acid-pepsin secretions. The most common forms of peptic ulcer are duodenal and gastric ulcer. Peptic ulcer disease, with its remissions and exacerbations, represents a chronic health problem. Ten percent of the population has or will develop peptic ulcer. Duodenal ulcers are two to three times more common than gastric ulcer. Ulcers in the duodenum occur at any age and are frequently seen in early adulthood. Gastric ulcers tend to affect the older age group, with peak incidence in the sixth and seventh decades. Both types of ulcer affect men three to four times more frequently than women.
Etiology
During the past 20 years, there has been a radical shift in thinking regarding the cause of peptic ulcer. No longer is peptic ulcer thought to result from a genetic predisposition, stress, or dietary indiscretions. Most cases of peptic ulcer are caused by H.pylori infection. The second most common form of peptic ulcer is from the use of NSAIDs, including aspirin.
Helicobacter pylori infection
Since its identification in 1982, H.pylori has generated worldwide interest. It has been reported that up to 85% to 100% of persons with duodenal ulcer and 70% to 90% of persons with gastric ulcer have H.pylori infection and active chronic gastritis.
Exactly how H.pylori and aspirin or NSAIDs lead to ulcer formation is unclear. Although they are independent risk factors, they may act synnergistically in causing ulcer and especially in the development of ulcer complications.
Nonsteroidal Antiinflammatory Drud-Induced Ulcers
There is a 10% to 20% prevalence of gastric ulcers and a 2% to 5% prevalence of duodenal ulcers among chronic NSAID users. Aspirin appears to be the most ulcerogenic of the NSAIDs. Ulcer development in NSAIDs users is dose dependent, but some risk occurs even with aspirin doses of 325 mg per day. The pathogenesis of NSAID-induced ulcers is thought to involve mucosal injury and inhibition of prostaglandin synthesis. In contrast to peptic ulcer from other causes, NSAID-induced gastric injury is often without symptoms, and life-threatening complications can occur without warning by the analgesic effects of the drugs that mask the ulcer symptoms.
Manifestations and Complications
The clinical manifestations of uncomplicated peptic ulcer focus on discomfort and pain. The pain, which is described as burning, or cramp like, is usually rhythmic and frequently occurs when the stomach is empty - between meals and at 1 o’clock or 2 o’clock in the morning. A peptic ulcer can affect one or all layers of the stomach or duodenum. The ulcer may penetrate only the mucosal surface, or it may extend into the smooth muscle layers. Occasionally, an ulcer penetrates the outer wall of the stomach or duodenum. Spontaneous remissions and exacerbations are common.
The complications of peptic ulcer include hemorrhage, obsrtuction, and perforation. Hemorrhage is caused by bleeding from granulation tissue or from erosion of an ulcer into an artery or vein. Evidence of bleeding may consist of hematemesis or melena. Acute hemorrhage is evidenced by the sudden onset of weakness, dizziness, thirst, cold moist skin, the desire to defecate, and the passage of loose, tarry, or even red stools and coffee-ground emesis. Signs of circulatory shock develop depending on the amount of blood that is lost. Obstruction is caused by edema, spasm, or contraction of scar tissue and interference with the free passage of gastric contents though the pylorus. There is a feeling of epigastric fullness and heaviness after meals. Perforation occurs when an ulcer erodes through all the layers of the stomach or duodenum wall. With perforation, gastrointestinal contents enter the peritoneum and cause peritonitis.
Treatment
• Helicobacter pylori eradication - combination of antibiotic therapy, proton pump inhibitors, and bismuth.
• Mucosal protective agents - bismuth and prostaglandin analogues
• Agents that decrease gastric acid content - neutralization of gastric acid - antacids; decrease in gastric acid production - H2-receptor antagonists or proton pump inhibitors.
Gastric Carcinoma
About 95% of stomach cancers are adenocarcinomas. Adenocarcinomas of the stomach originate from the glandular cells of the stomach lining.
Causes
Adenocarcinoma of the stomach often begins at a site where the stomach lining is inflamed. Helicobacter pylori infection is the cause of most stomach cancer. People who have certain gene mutations are also at risk.
Stomach polyps may become cancerous (malignant) and are thus removed. Adenocarcinoma of the stomach is particularly likely to develop if the polyps consist of glandular cells, if the polyps are larger than ¾ inch (2 centimeters), or if several polyps exist.
Certain dietary factors were once thought to play a role in the development of adenocarcinoma of the stomach. These factors included a high intake of salt, a high intake of carbohydrates, a high intake of preservatives called nitrates (often present in smoked foods), and a low intake of fruit and green leafy vegetables. However, none of these factors has proved to be a cause.
Symptoms
In the early stages, symptoms are vague and easily ignored. Early symptoms may mimic those of peptic ulcer disease, with burning abdominal pain. Therefore, peptic ulcer symptoms that do not resolve with treatment may indicate stomach cancer. The person may notice a feeling of fullness after a small meal (early satiety).
People may begin to feel full after eating sooner than they normally do. They may have weight loss or weakness caused by difficulty eating or by an inability to absorb some vitamins and minerals. Anemia, characterized by fatigue, weakness, and light-headedness, may result from very gradual bleeding that causes no other symptoms, from malabsorption of vitamin B12 (a vitamin needed for red blood cell formation), or from malabsorption of iron (a mineral needed for red blood cell formation) due to a lack of stomach acid. Uncommonly, a person may vomit large amounts of blood (hematemesis) or pass black tarry stools (melena). When adenocarcinoma is advanced, a doctor may be able to feel a mass when pressing on the abdomen.
Even in the early stages, a small adenocarcinoma may spread (metastasize) to distant sites. The spread of the tumor may cause liver enlargement, a yellowish discoloration of the skin and the whites of the eyes ( jaundice), fluid accumulation and swelling in the abdominal cavity ( ascites), and swollen lymph nodes. The spreading cancer also may weaken bones, leading to bone fractures.
Diagnosis Endoscopy and biopsy Computed tomography (CT) Endoscopic ultrasonography
Treatment
Surgery
Sometimes chemotherapy and radiation therapy
If the cancer has spread beyond the stomach, surgery cannot cure the condition, but it is sometimes used to relieve symptoms. For example, if the passage of food is obstructed at the far end of the stomach, a bypass operation, in which an alternate connection is made between the stomach and the small intestine, allows food to pass. This connection relieves the symptoms of obstruction—pain and vomiting—at least for a while.
