Peptic Ulcer Disease Treatment and Management

Beat Ulcers

The system is all natural and easy to use. You are just minutes away from taking your first steps to having painless days and nights. In less than 2 weeks, you can be totally free from ulcers, living without the pain and feeling free to eat without the thought of pain. All you need do is follow the plan. Beat Ulcers is a step by step guide that shows you how you can eliminate ulcers in as little as 10 days. All you need do is use the readily available natural products in the correct proportions at the correct times. Here is what you will learn in the Beat Ulcers guide: How to Eliminate an Ulcer without the use of medication. How to rid your body of the ulcer causing bacteria and keep it away. How to stop the aching. How to eliminate the burping and bloating. Focus on the root cause of ulcers rather than the symptoms. How to be totally free from pain and sleep soundly at night. How to stop using dangerous medications that are prescribed over and over. Learn the causes of ulcers and how to eliminate them forever.

Beat Ulcers Summary

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Complications and management of peptic ulcer surgery Early Complications

Cigarette smoking is detrimental to mucosal protective mechanisms and increases the likelihood that gastric ulcers will develop. Although these ulcers are generally amenable to ulcer treatment, they can occasionally be refractory to healing. This can be a difficult clinical problem in a patient with symptoms. If multiple biopsies have been negative for cancer, it is highly unlikely to be a malignant ulcer. As the ulcers will heal with cessation of smoking, this is the treatment of choice. The surgeon should be careful about offering a definitive ulcer operation in this patient group. Symptoms are often times not eliminated, and postgastrectomy complications are high. Giant Peptic Ulcer Giant peptic ulcers have traditionally been associated with a high complication rate and have been treated surgically. This is yet another area where surgical principles have changed. With treatment of H. pylori, and modern acid suppression, most giant ulcers can be healed medically (12). Surgery is...

Peptic Ulcer Disease

Peptic ulcer disease remains the most common cause of upper GI bleeding in most series, accounting for 35-50 of all cases if both gastric and duodenal ulcers are considered. Over the last 20 years, a number of advances in our understanding of the pathogenesis of peptic ulcer disease have altered the treatment and changed the role of surgery in this disease. With the elucidation of the role of H. pylori in ulcer pathogenesis and the advent of histamine antagonists, proton pump inhibitors, and therapeutic upper GI endoscopy, surgery for peptic ulcer disease has become much less commonplace. However, up to 15 of cases (6) are refractory to medical treatment and require surgical intervention. Indeed, patients requiring surgery today have problems that are more complex and associated with comorbidities and thus are more challenging for the surgeon. The indications for operative intervention for bleeding peptic ulcers remain the same as in the past (a) exsanguinating hemorrhage (b) active...

Phillip Chung md and Karen E Kim ms md

The overall incidence of upper GI bleeding is approximately 100 cases per 100,000 population (4,5). Acid peptic disease (e.g., gastric and duodenal ulcers as well as gastritis) is the most common cause of upper GI bleeding, accounting for 50-75 of all cases (6-8), even among patients with chronic alcohol use, portal hypertension, and varices (9). Furthermore, the predominance of peptic ulcer bleeding has not been affected by the advent of improved acid suppression with medical therapy (6). Acid peptic disease is followed by variceal bleeding, gastric and duodenal erosive disease, and Mallory-Weiss tears in prevalence, each accounting for approximately 15 of the overall incidence (8,10). The elderly appear to be at particular risk, as the proportion of elderly patients who present with upper GI bleeding has steadily increased, with persons older than age 60 years accounting for 35-45 of all cases (11). This increase cannot be explained by demographics alone, as increasing age directly...

H pylori Type IV Secretion Dependent Activation of Rac and Cdc42

H. pylori is associated with chronic superficial gastritis (stomach inflammation) and plays a role in the pathogenesis of peptic ulcer disease. Increasing evidence also indicates that H. pylori infection is important in promoting gastric carcinoma and lymphoma. Most of the time, however, chronic infection is asymptomatic. Despite gastric acidity, H. pylori proliferates in the mucus layer and a small proportion of cells (10 ) adheres to the gastric epithelium. The microorganism does not appear to invade tissue. Production of both a vacuolating cytotoxin (VacA) and the cag-encoded type IV secretion system is associated with injury to the gastric epithelium. In vitro, H. pylori infection activates Rac1 and Cdc42 1 h after infection (Churin et al. 2001). The cag-encoded secretion system is necessary for this process, suggesting that bacterial effectors secreted by the cag secretion system are responsible for the activation. CagA is the only known substrate of this secretion system, but...

Clinical Presentation

Abdominal pain is the principle symptom of peptic ulcer and is most commonly felt in the epigastrium. The quality of the discomfort, its pattern, and its associated symptoms such as vomiting may vary from patient to patient. In fact, the sensitivity and specificity of characteristic epigastric discomfort in predicting the presence of a peptic ulcer is actually quite low. Other possibilities in the differential diagnosis of ulcer pain include gastroesophageal reflux disease, angina, nonulcer dyspepsia, small and large intestinal conditions, gallstones, and pancreatic disorders. Furthermore, patients (especially those taking NSAIDs) frequently present with complications such as GI bleeding after a silent course and no pain. Nonetheless, there are classic symptomatic presentations in some patients that are worthy of mention. For example, the classic description of duodenal ulcer pain is a burning or gnawing sensation in the epigastrium, which characteristically occurs IV2-3 hours after...

Etiology Helicobacter pylori

In their landmark publication in 1983, Warren and Marshall (13) characterized H. pylori, a curved Gram-negative rod, and described its relationship to histologic gastritis. Subsequently, the organism was shown to satisfy Koch's postulates as an infectious cause of gastritis and was linked to peptic ulcer disease and gastric cancer. It is now recognized to be the cause of most acute and recurrent ulcers. Acquisition of infection appears to occur in early childhood and, although the evidence is only indirect, transmission of H. pylori is presumably via fecal-oral or oral-oral routes. Consequently, this mechanism is felt to explain the high prevalence of infection in children in developing nations who live in conditions of less than optimum sanitation. On the other hand, in developed nations with better living conditions and public health measures, children are less frequently exposed to infection. For example, in a U.S. study, the prevalence increased from approximately 10 at age 20...

Small GTPase Activation and Epithelium Destruction

It is not clear how tissue damage affects the infection process, but it could be important for evasion of the immune system or access to deeper tissues or for favoring bacterial dissemination to another host. In any case, it is thought to be involved in H. pylori-triggered pathological symptoms associated with epithelium destruction such as peptic ulcer and could be involved in cancer development, as the morphological changes induced by H.pylori resemble the process of oncogenic transformation.

Helicobacter pylori and NSAIDInduced Ulcers

In summary, because H. pylori and NSAIDs appear to produce ulcers by different mechanisms, and in the absence of sound evidence suggesting a therapeutic advantage, testing for H. pylori does not appear to be indicated for all patients starting on NSAID therapy. Patients with a preexisting history of peptic ulcer disease should be tested for H. pylori and treated with antibiotics if the test is positive in order to reduce recurrence of H. pylori-associated ulcers.

Clinical Box 11 Why Doesnt Your Stomach Digest Itself

The weakening of these mucosal defense mechanisms results in ulcerations and eventually gastric ulcer disease. A variety of factors including excessive alcohol and tobacco consumption, stress, and nonsteroidal anti-inflammatory drugs such as aspirin can lead to erosion in the lining of the stomach. Additionally, there is also a positive correlation between Helicobacter pylori (H. pylori) bacterial infection and the incidence of gastric and ulcers of the small intestine. H. pylori produces large quantities of the enzyme urease, which hydrolyzes urea to produce ammonia. The ammonia neutralizes the gastric acid in the bacteria's immediate environment thus protecting the bacteria from the toxic effects of its normally toxic acid environment. It is remarkable how some cells find a way to survive even in the deadliest environment.

Treatment Of Ulcers In Nsaid Users

Proton pump inhibitors are superior to H2RAs and misoprostol for healing NSAID ulcers in the setting of continued NSAID use. In the Acid Suppression Trial Ranitidine versus Omeprazole for NSAID-Associated Ulcer Treatment (ASTRONAUT) study, 541 patients with ulcers or extensive erosions were randomized to omeprazole 20 or 40 mg or ranitidine 150 mg twice daily. After 8 weeks of treatment, the rates of healing in all types of lesions were higher in those treated with omeprazole compared with ranitidine. The higher dose of the proton pump inhibitor was not superior to the lower dose (33). Similar data exist for other proton pump inhibitors (34). In the Omeprazole versus Misoprostol for NSAID-Induced Ulcer Management (OMNIUM) study, in which 900 NSAID using patients with ulcers or extensive erosions were randomized to receive misoprostol 200 g 4 times a day or omeprazole 20 or 40 mg once daily for 8 weeks, gastric ulcer healing was significantly more frequent on 20 mg of omeprazole...

Proton Pump Inhibitors

Given that high-dose acid suppression with H2RAs prevents NSAID ulcers in the stomach and duodenum, it follows that more potent proton pump inhibitors should be more effective. Omeprazole has proved effective in primary prophylaxis of NSAID-induced ulcers compared with placebo in a study of 169 patients requiring continuous NSAID therapy (41). After 6 months, 78 of the omeprazole group remained in remission, compared with 53 in the placebo group (p 0.004). There were three gastric ulcers and no duodenal ulcers in the omeprazole group, compared with eight and three, respectively, in the placebo group (35). In the ASTRONAUT study (33), patients requiring continuous NSAID therapy were randomized, following ulcer healing, to receive ranitidine (150 mg bid) or omeprazole 20 mg daily. Gastric ulcers recurred in 5.2 of the omeprazole-treated patients versus 16.3 of those in the ranitidine-treated group (p 0.001). For duodenal ulcers, there was a 0.5 versus a 4.2 (p 0.02) rate of recurrence...

Spectrum Of Disease

Has also been reported to cause septicemia, cellulitis, and meningitis in immunocompromised patients. H. pylori causes gastritis, peptic ulcer disease, and gastric cancer.4,6 However, most individuals tolerate the presence of H. pylori for decades with few, if any, symptoms.

H pylori Genomics and Virulence

Many of the defined H. pylori virulence determinants such as flagella, motility, and urease activity, are found in all strains (4,5). Conversely, the immunodominant cyto-toxin-associated gene antigen, CagA, and the vacuolating cytotoxin, VacA, are present in some strains and absent in others. Although CagA and VacA are now known to be unlinked, strains that possess the cagA gene frequently express a functional vacA gene, and these strains are more frequently associated with peptic ulcer disease or cancer than strains without cagA that don't express vacA (72). CagA is now known to be part of, and the only identified substrate of, a type IV secretion system (72,73). Type IV secretion systems are ancestrally related to Gram-negative bacterial conjugation systems, and are used by pathogens to deliver protein substrates into eukaryotic host cells (74). No type III secretion system, which are used by Salmonella, Shigella, Yersinia, and enteropathogenic and enterohemorrhagic Escherichia coli...

When things go wrong in life

Eventually, though, after a series of questions about her diet and about whether she had had any history of stomach ulcers, she again became aggressive, even shouting at the doctor about there never having been anything like that in her family. And so it went on after they had admitted her. Each day, she would spend some time being almost obsequiously pleasant to some people, getting them clearly on her side, but then would round on them, throwing back any act of kindness shown to her in an almost vicious way.

Gastrointestinal Infections Helicobacter pylori

H. pylori is the causative agent of chronic active gastritis and peptic ulcer disease (78,79). H. pylori are also implicated in about 70 of gastric ulcers and there is increasing evidence to indicate its association with the development of gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. This infection is common in the general population, with most infected individuals being asymptomatic. Currently, combination therapy aimed at H. pylori is known to cure and to prevent recurrence of peptic ulcer disease and gastritis. Therapy has also been associated with regression of gastric MALT lymphoma. recommend treatment for 10 to 14 days because of inconsistent results in trials in the United States with 7-day therapy. Some U.S.-based randomized trials have demonstrated that there was no statistical difference between eradication rates in 7-day regimens versus 14-day regimens (89). But the 7-day regimen had a numerically lower eradication rate and it was...

Adverse Effects of Systemic Glucocorticoid Therapy

As all nucleated cells in the body have a common GC receptor, all are potentially affected by GC therapy and thus susceptible to the development of untoward effects. These effects can occur immediately (i.e., metabolic effects) or can develop insidiously over several months to years (i.e., osteoporosis and cataracts). In addition, some adverse effects are limited to children (growth suppression) while others appear to require interaction with other drugs (nonsteroidal anti-inflammatory agents and peptic ulcer disease). Most adverse effects occur in a dose-dependent and duration-of-treatment manner, although this has not been uniformly noted. Table 3 lists many of the common adverse effects associated with chronic GC use. tional lability to frank psychosis can occur, as well as hypertension, peptic ulcer disease, atherosclerosis, aseptic necrosis of bone, and diabetes mellitus. Chronic GC use can also result in immunologic attenuation with loss of delayed type hypersensitivity,...

Multiple Endocrine Neoplasia Type

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant cancer syndrome that features tumors of the parathyroid, pituitary, and the islet cells of the pancreas. These tissues are part of the endocrine system, which produces and secretes various hormones. In response to different hormones, target cells control homeostatic processes, growth, development, and stress. Specifically, with regard to the sites of the MEN1 tumors, the parathyroid glands control levels of calcium and phosphate the pituitary glands regulate metabolic activities of other endocrine glands and growth and the pancreatic islet cells maintain blood glucose concentration. Depending on the site and the extent of the MEN1 tumors, symptoms may include excess calcium in the bloodstream (hypercalcemia), which causes kidney stone formation low blood sugar concentration (hypoglycemia), resulting in dizziness, confusion, weight loss, and glucose intolerance and disruption of the pituitary gland, accompanied by...

Acute Upper Gastrointestinal Hemorrhage

The causes of upper GI hemorrhage (Table 1), in order of decreasing frequency, are peptic ulcer disease (Fig. 1), portal hypertensive variceal bleeding (Fig. 2), Mallory-Weiss tears, angiodysplasias, gastric neoplasms, and erosive gastritis esophagitis (11). Despite medical advances in prevention and management, peptic ulcer disease remains the most common cause of bleeding in the upper GI tract, accounting for almost half of all cases presenting with severe hemorrhage (12-15). Dieulafoy's lesion Gastric ulcer Hemorrhagic gastritis Duodenum coagulation therapy and or injection of a vasoconstrictive agent into an actively bleeding ulcer or visible vessel have been shown to reduce the rate of rebleeding significantly (16,17). When endoscopy fails to identify or control the source of bleeding, the assistance of interventional radiology and or surgery may be required.

Milijana Knezevic Sanja Aleksic Kovacevic and Zoran Aleksic

Esophagogastric ulcer is an independent disease in swine that is characterized by ulcerous autodigestion of the cutaneous mucosa, which does not exhibit a tendency to recover, but, on the contrary, a tendency toward severe hemorrhaging, with a predominantly lethal outcome. Since it develops in the part of the stomach that is morphologically and functionally different from other glandular mucosa, it was questioned earlier whether it could be a peptic ulcer based on its nature. Spontaneous ulcers, usually of the stomach, commonly occur in many domestic animals. Some of these lesions are chronic and they may occur in either the glandular or squamous-lined regions of the stomach. As with the human disease, the pathogenesis in domestic animals is multifactorial, poorly understood, and variable between and within species. Environmental stress and dietary factors are very important in the ulcer disease in swine. It has been shown that the Helicobacter spp. is strongly associated with...

Emerging bacterial diseases

Among the constant challenges in managing bacterial infections are the outbreak of new infectious diseases and the evolution of known commensal and pathogenic bacteria to problem status by acquisition of new resistance determinants. A National Academy of Sciences report, Emerging and Re-emerging Diseases Global Microbial Threats in the 1990s, listed infectious diseases that have become recognized since 1973 (Davis and Lederberg, 2000). The bacterial diseases in that category are excerpted in Table 17.1 and include the toxic shock syndrome forms of S. aureus, Legionella pneumophila, and peptic ulcer-causing Helicobacter pylori. In a world of global travel and change of habitats, new diseases emerge. Once identified, most are currently treatable with existing antibiotics, but that will start the accelerated path to evolution of drug resistance. In companion, for newly emerging viral diseases there may be no available therapies. Cohen (2000) notes that changes in societal patterns...

Some Edible Vegetables Of Saponin Containing Indigenous To China

Buds of tender leaves contained triterpene saponins from which genins were obtained after hydrolysis, they were barringtogenol C and Rl-barrigenol, along with cinnamic acidangelic acid, tiglinic acid, arbinose, xylose, galactose andglucuronic acid etc.The tender leaves have the effects toimprove eyesight, relieve excessive thirst, dissipate phlegm, promote digestion of diuretic and detoxication. The saponinshave the effects of antifungus, microrganismcide, anti-inflamation antigonizing of atherosclerosis, provention and treatment of hypertension antagonizing of gastric ulcer and anticarcinogen. Saponins from fermented wulun tea was used as toniz, as well as it's extract has the effect of litholysisin urethra and nontoxic for long time administration.

Peg Vs Radiological Or Surgical Gastrostomy

Inadvertent and premature removal of the PEG prior to tract maturation results in peritonitis in 0-1 of cases. It may likewise result from perforation of a viscus, preexisting gastric ulcer and leakage around the gastrostomy site. Emergent operative management is indicated in the presence of fever, leukocytosis, abdominal pain, and tenderness. In the absence of peritoneal signs, immediate PEG replacement may be accomplished endoscopically . If the location of the tube remains in question, a fluoroscopic study with a water-soluble contrast agent infused through the PEG should be performed to confirm tube position and to demonstrate the presence or absence of a leak (15). Hemorrhage is a rare complication of PEG placement and occurs in 0-2.5 of cases. It may result from trauma to the esophageal or gastric mucosa, peptic ulcer disease, or trauma to a gastric vessel. Therapy is aimed at applying traction with the internal bumper to tamponade the bleeding vessel, and correcting any...

Current surgical treatment of ulcer complications

Posterior Gastric Ulcer Artery

The primary treatment of bleeding ulcers is endoscopic control followed by treatment for H. pylori if present. Even rebleeding is best treated by repeat attempts at endoscopic control (4). Surgery is indicated for significant bleeding (requiring over five units of blood) that cannot be controlled by endoscopy. Most uncontrolled bleeding ulcers are from the gastroduodenal artery in the posterior aspect of the duodenal bulb. Treatment is by duodenotomy, and ligation of the bleeding site (Fig. 6). The integrity of the pylorus should be preserved. Gastric ulcers should be treated with ulcer excision if amenable. Ulcers located in regions difficult to excise (cardia, prepyloric) should be biopsied and oversewn. Occasional large or penetrating ulcers may be best treated with distal gastrec-tomy for technical considerations or to rule out cancer. Patients with ulcer perforation should be assumed to be H. pylori positive unless there is evidence to the contrary. Duodenal ulcers and prepyloric...

Zhongming Ge and David B Schauer

Helicobacter pylori was the first bacterial species to have the genome of two independent strains completely sequenced. Infection with this pathogen, which may be the most frequent bacterial infection of humanity, causes peptic ulcer disease and gastric cancer. Other Helicobacter species are emerging as causes of infection, inflammation, and cancer in the intestine, liver, and biliary tract, although the true prevalence of these enterohepatic Helicobacter species in humans is not yet known. The murine pathogen Helicobacter hepaticus was the first enterohepatic Helicobacter species to have its genome completely sequenced. Here, we consider functional genomics of the genus Helicobacter, the comparative genomics of the genus Helicobacter, and the related genera Campylobacter and Wolinella. Key Words Cytotoxin-associated gene e-Proteobacteria gastric cancer genomic evolution genomic island hepatobiliary peptic ulcer disease type IV secretion system.

Postgastrectomy syndromes

Gastrojejunostomy With Truncal Vagotomy

The most important common postgastrectomy syndromes are dumping, alkaline reflux gastritis, and gastric stasis. Less common postgastrectomy syndromes include small stomach syndrome, postvagotomy diarrhea, afferent loop syndrome, efferent loop syndrome, and recurrent ulcer. Most patients also develop iron deficiency anemia likely caused by exclusion of the duodenum from the enteral stream. The duodenum is the primary site of iron absorption. Poor mixing of the bile and food can result in malabsorption. B12 and folate deficiencies are common nutritional complications. Owing to the hypochlorhydria following vagotomy, postgastrectomy patients may be at greater risk for developing cancer in the gastric remnant. The incidence of postgastrectomy syndromes has decreased overall as a result of the marked decrease in the number of gastric surgeries performed, especially for peptic ulcer disease. This is mainly because of the recognition of H. pylori and its causal relationship with peptic ulcer...

Roux -en Y Bypass Surgery Indications

The usual indications for a bypass are obstruction by a benign or a malignant stricture. Benign strictures are particularly likely to occur in the distal bile duct as a result of stones, or chronic pancreatitis. Benign strictures in the middle of the of the common duct, up to and including the bifurcation can also be caused by stones, parasitic infestations, autoimmune inflammation of the ducts (e.g., sclerosing cholangitis), congenital problems (e.g., Caroli's disease), or even trauma. However, the most common reason is iatrogenic the most notorious of these in modern times being an operative injury during laparoscopic cholecystectomy. The injury may occur by transaction, inadvertent clip placement, cauterization or indirectly by devascularization of the duct. Because the blood supply to the mid-bile duct is axial (Fig. 3), it is relatively susceptible to devascularization. The injury may or may not be recognized at the original surgery. If it is recognized and repaired simply by...

Longstreth 1991 Gi Bleeding

Kubba AK, Choudari C, Rajgopal C, Palmer KR. The outcome of urgent surgery for major peptic ulcer haemorrhage following failed endoscopic therapy. Eur J Gastroenterol Hepatol 1996 8 1175-1178. 8. Lau JY, Sung JJ, Lam YH, et al. Endoscopic retreatment compared with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding ulcers. N Engl J Med 1999 340 751-756. 10. Morris DL, Hawker PC, Brearley S, Simms M, Dykes PW, Keighley MR. Optimal timing of operation for bleeding peptic ulcer prospective randomised trial. BMJ (Clin Res Ed) 1984 288 1277-1280. 11. Ohmann C, Imhof M, Roher HD. Trends in peptic ulcer bleeding and surgical treatment. World J Surg 2000 24 284-293. 12. Poxon VA, Keighley MR, Dykes PW, Heppinstall K, Jaderberg M. Comparison of minimal and conventional surgery in patients with bleeding peptic ulcer a multicentre trial. Br J Surg 1991 78 1344-1345.

Helicobacter pylori

The association of Helicobacter pylori with peptic ulcer disease and gastric cancer was first proposed by Warren and Marshall in 1983 (Warren and Marshall, 1983). In February 1994, the National Institutes of Health Consensus Development Conference concluded that H. pylori infection is the major cause of peptic ulcer disease, and all patients with confirmed peptic ulcer disease associated with H. pylori infection should receive treatment with antimicrobial agents (Yamada et al., 1994). The International Agency for Research on Cancer Working Group of the World Health Organization categorized H. pylori as a group I, or definite, human carcinogen (Versalovic, 2003). Based on the data retrieved during the National Health Interview Survey of 1989, 10 of adult U.S. residents reported physician-diagnosed ulcer disease, among whom one third had an ulcer in the past year (Sonnenberg and Everhart, 1996). In developing countries, the prevalence of H. pylori carriers can be as high as 70-90 . Most...

Reflux Esophagitis

In several series, reflux esophagitis accounted for only 2-5 of all cases of acute upper GI bleeding, occurring less commonly than peptic ulcer disease (57-75 ), esophageal varices (7-9 ), or Mallory-Weiss tears (19,20,33,34). However, in one recent study, reflux esophagitis accounted for 14.6 of overt upper GI tract bleeding (35). The bleeding associated with acid reflux is not typically massive. In two large series, there were no deaths attributed to bleeding from reflux esophagitis (19,20).

Epidemiology

At the end of the 1980s, it was estimated that approximately 500,000 new cases of peptic ulcers occurred annually in the United States, and the lifetime risk of peptic ulcer disease was estimated at 5-10 (1). More recent estimates of prevalence have been similar, at least 10 of Americans having a history of peptic ulcer disease (2), with acute exacerbations annually leading to 8 million physician visits and 275,000 hospitalizations for a total of 3 million hospital days (3). Traditionally peptic ulcer disease has been a disease of younger men, but now it appears to affect women and the elderly more frequently. Although overall hospitalization rates for peptic ulcer disease have decreased over the last several decades, hospitalizations (especially of elderly patients with ulcer-related complications such as bleeding and perforation) have increased (4-6).

Diagnosis

Since history may not accurately predict ulcer disease, diagnostic testing is often necessary. Upper GI endoscopy esophagoduodenoscopy (EGD) is the most accurate test for diagnosing ulcers of the stomach and duodenum. A study comparing double-contrast barium upper GI X-rays with endoscopy found the diagnostic accuracy of upper GI series to be 65 and that of endoscopy 88 (7). Unlike X-ray studies, endoscopy also allows biopsy of gastric ulcers to exclude cancer and for the detection of H. pylori. The location of a duodenal ulcer could be important in suggesting a possible cause. Most ulcers of the duodenum occur in the duodenal bulb. Postbulbar ulcers can occur in those infected with H. pylori or those using NSAIDs, but their presence should raise the possibility of other conditions such as gastrinoma or unusual infections in the appropriate patient.

Other Causes

Gastrinoma (Zollinger-Ellison syndrome), infections such as syphilis and tuberculosis, opportunistic infections such as cytomegalovirus and herpes simplex virus in immunosuppressed patients, and Crohn's disease are rare causes of ulcers in the upper GI tract. Neoplasm must be considered in the appropriate patient with gastric ulcer. True idiopathic ulcers also occur. Some such lesions are thought to be heredi

Operative techniques

Producing parietal cells, but the grinding function of the antrum and the emptying ability of the pylorus are preserved. Proximal gastric vagotomy (also called highly selective vagotomy or parietal cell vagotomy) was technically more demanding, and high recurrent ulcer rates were seen until the procedure was standardized. Once all the nuances of the procedure were appreciated, recurrent ulcer rates were 10 or less and postgastrectomy side effects were much less than those seen with vagotomy and pyloroplasty (3). Proximal gastric vagotomy was not as effective for gastric ulcers and was not used by most surgeons for this indication.

Treatment

Acid suppression to promote mucosal healing, removing offending agents such as aspirin or NSAIDs (49-60), and treating H. pylori if present are the principles of ulcer treatment. H2 receptor antagonists can heal peptic ulcers, but PPIs are more effective and are associated with higher and faster healing rates for both gastric and duodenal ulcers (6164). Most uncomplicated duodenal and gastric ulcers heal after once-daily dosing of PPIs for 4 and 8 weeks, respectively. Actually, in some duodenal ulcer patients with H. pylori infection, the duration of antisecretory therapy may be limited to the duration of the H. pylori regimen, which is commonly 2 weeks. Factors that may influence the decision to extend antisecretory therapy beyond 4-8 weeks include persistent symptoms, size of ulcer, presence of complicating factors such as bleeding, and potentially concomitant aspirin or NSAID use. Indeed, twice-daily PPI dosing for at least 8 weeks is appropriate to ensure healing of complicated...

Bleeding

Peptic ulcer is the most common cause of acute upper GI bleeding and accounts for approximately 50 of all upper GI bleeding cases (84). There are approximately 150,000 hospitalizations per year in the United States for evaluation and treatment of bleeding ulcers. Although hospitalization and surgery for uncomplicated ulcers have decreased in the United States and Europe over the past three decades, the number of hospitalizations for hemorrhage associated with ulcers has remained unchanged (85). Even though ulcer bleeding stops spontaneously in at least 80 of patients, the overall mortality is also unchanged over the last 30 years, ranging from 6 to 7 in the United States (85) and averaging 14 in the United Kingdom (86). Without specific hemostatic intervention, peptic ulcer bleeding continues or recurs in approximately 20 of patients (87). Clinical and endoscopic prognostic indicators are shown in Table 2. With regard to age, the mortality of ulcer bleeding in those older than 60...

Summary

The most common cause of peptic ulcer is H. pylori infection. Peptic ulcer can present silently with complications such as hemorrhage, particularly in patients on NSAIDs. PPIs are the mainstays of therapy and should be held prior to noninvasive diagnostic tests for H. pylori. Effective eradication of H. pylori involves regimens utilizing multiple antibiotics. COX-2 inhibitors have lower incidence of causing peptic ulcers. Upper endoscopy effectively diagnoses peptic ulcers, reduces rebleeding, and allows for appropriate triage of patients with upper GI bleeding complications. Figure 1 summarizes an algorithmic approach to bleeding peptic ulcer disease.

Emotions and health

Emotion can be involved in any medical condition. For example, a broken leg can lead to anger and frustration, anxiety, fear, sadness, and so on. Or it may be that one's emotional condition was a precipitating factor in whatever led to the leg being broken in the first place. But the most problematic circumstance comes with the idea of psychosomatic disorders, in which the disorder is clearly physical (migraine, skin rashes, indigestion, peptic ulcers, asthma, genito-urinary conditions, and so on) but the causative factors seem to be emotional. The emotion most commonly implicated is anxiety. The extent of the emotional is hard to determine, one view being that all illness has an emotional component, causa-tively. For example, long-term stresses may well have a deleterious impact on the efficacy of the immune system and thus leave a person more vulnerable to infection.

Etiology

Upper GI lesions found in patients with obscure bleeding include peptic ulcer disease in 0-11 , erosions within large hiatal hernias (Cameron's erosions 0-8 ), and gastric or duodenal vascular malformations in 0-8 . Less common upper tract sources of obscure bleeding are esophagitis, esophageal ulcer, esophageal varices, gastric or duodenal polyps, Dieulafoy's lesion, gastric antral vascular ectasia (GAVE also known as watermelon stomach), blue rubber bleb nevus syndrome, Osler-Weber-Rendu syndrome, and celiac sprue (Table 1).

Evaluation

In one study of 17 patients with obscure blood loss, 35 had a bleeding source identified on repeat endoscopy (upper endoscopy 29 , colonoscopy 6 ) (22). Even when the intent is to examine the small bowel with an enteroscope, a source that should have been discovered at the prior endoscopy was found in 28-75 of patients in whom a diagnosis was made by enteroscopy (23). The most common lesions missed during upper endoscopy include erosions within large hiatal hernias (Cameron's erosions), peptic ulcer disease, and vascular ectasia. However, one report of 39 patients with obscure bleeding found no additional diagnostic yield when upper endoscopy and colonoscopy were repeated.

Other Diseases

In coronary balloon angioplasty, increased extracellular matrix deposition frequently occurs, leading to restenosis. Studies have shown increased type I collagen production following experimental angioplasty, as well as decreased MMP activity (119). The broad-spectrum MMP inhibitor Galardin 2 reduced both collagen synthesis and degradation in an iliac artery model of restenosis following balloon angioplasty. Increased matrix turnover has also been linked to the destabilization of atherosclerotic plaques (120), and elevated gelatinase-B activity has been implicated as a causative factor in the enlargement of abdominal aortic aneurysms (40). Other diseases that have been considered as targets for MMP inhibitor therapy include emphysema (121), gastric ulcers (122), and inflammatory bowel disease (123). In each case, there is evidence to suggest that MMPs secreted by inflammatory or stromal cells are responsible for the tissue remodeling and degradation that occurs in these conditions.

Late Complications

The most frustrating problem that faces the surgeon is the patient who has undergone cholecystectomy and returns with symptoms identical to those prior to surgery. The return of episodic upper abdominal pain after cholecystectomy may indicate other underlying pathology such as peptic ulcer disease or pancreatitis, or even angina. A search for other conditions should be undertaken. There is also the possibility that the patient has common bile duct stones. These can certainly mimic the symptoms that precipitated the cholecystectomy in the first place. Common bile duct stones that develop in the bile duct after cholecystectomy are known as primary common bile duct stones. These are typically soft brown crumbly stones that occur in an abnormal, poorly emptying duct. More commonly, post cholecystectomy common bile duct stones are retained stones stones that came from the gallbladder before it was removed.

What is abnormal

Balance can vary from time to time and person to person within one disorder. For example, a stomach ulcer might have its main cause in the food eaten or it might have its main cause in living a stressful life. Whatever the balance of causes, it remains a stomach ulcer. So, to say to someone 'It's just psychological' or 'It's all in your mind' is nonsense.

Angiography

The overall yield of angiography is 40-78 (15). Diverticular disease and angiodysplasia are the most common findings (15-18). Other lesions include peptic ulcer, Meckel's diverticulum, neoplasm, and vascular-enteric fistula. Angiography may also define lesions with abnormal vasculature, such as vascular malformations or tumors, even if extravasation of contrast material is not noted. This is useful in patients with acute massive bleeding that has slowed by the time of angiography or in patients with chronic or recurrent bleeding in whom a diagnosis has been difficult to establish. A bleeding rate of 1 mL min during angiography is generally required for a positive result, much higher than that needed for scintigraphy (as low as 0.1 mL min) (19,20), although rates as low as 0.4 mL min have been detected.

Non Opioid Analgesics

Unlike opioid analgesics, the non-opioid analgesics have a 'ceiling' effect for analgesia and produce neither tolerance nor physical dependence. Some of these agents, like acetylsalicylic acid and the NSAIDs, inhibit the enzyme cyclo-oxygenase and consequently block the biosynthesis of pros-taglandins, inflammatory mediators known to sensitize peripheral noci-ceptors 43-45 . A central mechanism is also likely and appears to predominate in acetaminophen analgesia, because its action on PGE2 synthesis. The safe administration of the non-opioid analgesics requires familiarity with their potential adverse effects. Acetylsalicylic acid and the other NSAIDs have a broad spectrum of potential toxicity. Bleeding diathesis due to inhibition of platelet aggregation, gastroduodenopathy (including peptic ulcer disease) and renal impairment are the most common 46-50 . Less common adverse effects include confusion, precipitation of cardiac failure and exacerbation of hypertension. Particular...

Gastritis

Gastritis refers to inflammation of the gastric mucosa. This illness is associated with nausea and upper abdominal pain vomiting, burping, and fever may also be present A curved organism called Helicobacter pybri is seen on the surface of gastric epithelial cells of patients with gastritis. The organism is recovered from gastric biopsy material obtained endoscopically but not from stool. Following acute infection, H. pylori can persist for years in most individuals, with most remaining asymptomatic. H. pybri is also the causative agent of peptic ulcer disease and a significant risk factor for stomach cancer.

Adjuvant Analgesics

Significantly improve quality of life and to have beneficial effects on appetite, nausea, mood and malaise. The mechanism of analgesia produced by these drugs may involve anti-oedema effects, anti-inflammatory effects and a direct influence on the electrical activity in damaged nerves. The relative risks and benefits of the various corticosteroids are unknown and dosing is largely empirical. In the United States, the most commonly used drug is dexamethasone, a choice that gains theoretical support from the relatively low mineralocorticoid effect of this agent. Dexamethasone has also been conventionally used for raised intracranial pressure and spinal cord compression. Prednisone, methylprednisolone and prednisolone have also been widely used for other indications. Patients who experience pain and other symptoms may respond favourably to a relatively small dose of cortico-steroid (e.g. dexamethasone 1-2 mg twice daily). In some settings, however, a high-dose regimen may be appropriate....

Misoprostol

Prostaglandin depletion is central to the development of NSAID ulcers thus replacement therapy with a synthetic prostaglandin would be expected to reduce NSAID toxicity. Well-designed placebo-controlled studies (37) have demonstrated the efficacy of the prostaglandin E1 (PGE1) analog misoprostol for the prevention of endoscopic ulcers in NSAID-using arthritis patients. Misoprostol is the only agent currently available with well-established prophylactic efficacy for the prevention of NSAID-associated serious GI complications (e.g., bleeding, perforation, obstruction). The MUCOSA trial (16) identified a 40 relative risk reduction. Misoprostol cotherapy appears to be cost-effective in high-risk patients only. The number needed to treat is 264, that is, 264 chronic NSAID-using patients need to be treated for 6 months to prevent a single definite upper GI complication (38). However, certain subgroups have an increased risk of serious upper GI complications, and the use of misoprostol would...