Treatments for Peptic Ulcer Disease

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


4.6 stars out of 11 votes

Contents: EBook
Author: Tammy Myers
Price: $29.99

My Beat Ulcers Review

Highly Recommended

I usually find books written on this category hard to understand and full of jargon. But the author was capable of presenting advanced techniques in an extremely easy to understand language.

This ebook served its purpose to the maximum level. I am glad that I purchased it. If you are interested in this field, this is a must have.

Download Now

Gastric Secretion Peptic Ulcer and Anticholinergics as Antiulcer Agents

Histamine Gastric Ulcer

The pathophysiologyof peptic ulcer is not fully known and, in the present state of knowledge, it is not possible to present the pertinent normal physiology briefly. For a detailed discussion on the physiology and chemistry of gastric secretion and the pathologic physiology of peptic ulcer, reference should be made to reviews on the subject (1-5). The following is a brief summary of the gastric secretion and its relationship to peptic ulcer, a knowledge of which is necessary to understand the problems of developing antiulcer agents. Peptic ulcer occurs in the pyloric region of the stomach or the first few centimeters of the intestine. The gastroduodenal muscosa is exposed constantly to mechanical, physical, and chemical insults, some of which have already been described. A peptic ulcer does not develop without the presence of a pepsin-containing juice of such low pH that it can exert a peptic The healthy stomach does not digest itself. Counteracting the aggression are defensive factors...

Approach To Peptic Ulcer Disease Definitions

Peptic ulcer disease (PUD) Presence of gastric or duodenal ulcers as demonstrated by endoscopy or by upper gastrointestinal barium study. The classic symptoms of duodenal ulcers are caused by the presence of acid without food or other buffers. Symptoms are typically produced after the stomach is emptied but food-stimulated acid production still persists, typically 2-5 hours after a meal. They may awaken patients at night, when circadian rhythms increase acid production. The pain is typically relieved within minutes by neutralization of acid by food or antacids (e.g., calcium carbonate, aluminum-magnesium hydroxide). Gastric ulcers, by contrast, are more variable in their presentation. Food may actually worsen symptoms in patients with gastric ulcer, or pain might not be relieved by antacids. In fact, many patients with PUD have no symptoms at all. Gastric cancers may present with dysphagia if they are located in the cardiac region of the stomach, with persistent vomiting if they block...

Treatment Of Nsaidinduced Peptic Ulcers

Withdrawal of NSAIDs and acid suppression with standard doses of antisecretory drugs will allow prompt resolution of these ulcers, which should not recur unless the drugs are resumed. Many patients are prescribed NSAIDs inappropriately when their symptoms could be controlled by paracetamol or by local treatment. Topical NSAID creams applied over an affected joint may be helpful, but peptic ulcers can complicate therapy with NSAIDs administered as rectal suppositories. Prodrugs such as sulindac, which are metabolised to form antiinflammatory derivatives, can also produce ulcers.

Prevention Of Nsaidinduced Peptic Ulcers

This is particularly relevant for the elderly and other high-risk patients (see above). The synthetic prostaglandin misoprostol in a dose of 800 micrograms daily in 2-4 divided doses reduces the incidence of gastric and duodenal ulceration and their complications by about 40 when coadministered with NSAIDs. Abdominal pain and diarrhoea limit its use halving the dose reduces the incidence of adverse effects, but at the expense of a reduced protective effect. The proton pump inhibitors, in healing doses, are similar in efficacy to the higher dose of misoprostol. H2 receptor antagonists offer some protection against duodenal ulcers but none against gastric ulcers. Selective inhibition of COX-2 has the objective of preserving anti-inflammatory activity whilst avoiding gastric mucosal toxicity. Rofecoxib, celecoxib and meloxicam vary in their selectivity for COX-2. The incidence of peptic ulcers and their complications with rofecoxib is similar to that seen when proton pump inhibitors are...

Peptic Ulcer

Peptic ulcers are small erosions in the wall of the stomach or duodenum. These areas are normally protected from gastric acid by mu-cosal secretions that form a protective barrier. When this barrier breaks down, damage occurs and an ulcer forms. Symptoms are pain, nausea, and bleeding. Ulcers are common, occurring in about one in 15 adults. The causes are multiple stress, poor diet, food sensitivities, and infection of the stomach by Helicobacter pylori can all contribute. Optimum nutrition can maintain the health of the protective lining of the stomach and duodenum. It can also support the immune system to increase resistance to chronic Helicobacter infection.

Classic Clinical Problem Solving

For example, a patient who complains of upper abdominal pain and has a history of nonsteroidal antiinflammatory drug (NSAID) use may have peptic ulcer disease another patient who has abdominal pain, fatty food intolerance, and abdominal bloating may have cholelithiasis. Yet another individual with a 1-day history of periumbilical pain that now localizes to the right lower quadrant may have acute appendicitis.

Nonanticholinergics As Antiulcer Agents

The interplay of various neuronal, hormonal, and other factors in gastric acid secretion are shown in Fig. 3.1. Pharmacological agents can be used to decrease gastric acid secretion by their action at different sites. So far, the principal medications other than anticholinergics and antiacids to treat peptic ulcer are limited. Experimental and clinical investigations are in progress on a number of agents that can decrease the volume and acidity of gastric secretion through mechanisms other than blockade of the cholinergic nervous system (264-267). These include (1) histamine H2-receptor antagonists (266), (2) gastrin inhibitors (265), (3) pepsin inactivators (265), (4) mucus producers (69), (5) prostaglandin analogs (69), (6) enterogastone and its analogs (265,267), (7) noncholinergicantispasmodics (69, 264), and (8) gastric H+ K+-ATPase inhibitors. Histamine H2 receptor antagonists are popular for the treatment of peptic ulcer (266). A single dose of cimitidine, an H2 receptor...

Gastrointestinal system

The gastrointestinal system is also affected by the spinal cord injury. Newly injured patients are at increased risk of developing stress related gastric ulcers and are regularly offered anti-acid treatment. It might be that the unopposed vagal outflow plays a role and increases the risk of ulcer formation. Other problems from the intestinal system are obvious to the patient soon after injury. The bowel is silent and the voluntary control of bowel emptying is lost. This paralytic ileus ceases within 1-2 weeks, but if liquids or solid food is given prior to this there is a clear risk of a prolonged period of paralytic ileus, with the concomitant risk of nausea and vomiting. A patient who is placed in skull traction is hard to manage properly during vomiting and there is a great risk of aspiration. Furthermore, a paralytic ileus could give rise to a meteoristic abdomen, which might interfere with respiration by interference with the breathing movement of the diaphragm.

Reversible Proton Pump Inhibitors

A tetrahydroisoqunoline-based compound, YH-1885, discovered by Yuhan, is currently one of the most clinically advanced reversible proton-pump inhibitors (170). It is now being codeveloped with GlaxoSmithKline for stomach ulcers and gastroesophageal reflux disease. Clinical data on YH-1885 have demonstrated that it is safe and well tolerated when administered as a single dose (60 to 300 mg) or multiple doses (150 to 300 mg) to healthy volunteers. The compound significantly increased gastric pH and increased the fraction of time above pH 3 at doses above 150 mg. During multiple dosing, YH-1885 exhibited a reversible mode of action with no significant

Cinnamon And Mydriasis

Peptic ulcer Same as above Production of chronic experimental peptic ulcers in dogs (or rats) by the Mann-Williamson procedure (36) is one of the standard methods. The gastric juice is diverted into the intestine some distance from the pancreatic and biliary secretions. The objective is achieved by isolating the duodenum from the pylorus and the jejunum. The oral end of the duodenum is closed and its distal end is anastomosed with a loop of ileum, so as to discharge the pancreatic and biliary secretions into the lower portion of the bowel. The cut end of the jejunum is then anastomosed to the pylorus. About 95 of dogs so prepared develop typical chronic peptic ulcers just distal to the gastric anastomosis with the jejunum. With similar operative procedures 85 of rats develop gastric, marginal, or jejunal ulcers. The complete reversal of the duodenum in dogs produces chronic peptic ulcers in about 6 months (19). These animals maintain their weight until the development of ulcerations...

Clinical features

Annular Pancreas Image

3 Anterior to the pancreas lies the stomach, separated from it by the lesser sac. This sac may become closed off and distended with fluid either from perforation of a posterior gastric ulcer or from the outpouring of fluid in acute pancreatitis, forming a pseudocyst of the pancreas. Such a collection may almost fill the abdominal cavity.

The subphrenic spaces

The right and left subhepatic spaces lie below the liver. The right is the pouch of Morison and is bounded by the posterior abdominal wall behind and by the liver above. It communicates anteriorly with the right sub-phrenic space around the anterior margin of the right lobe of the liver and below both open into the general peritoneal cavity from which infection may track, for example, from a perforated appendix or a perforated peptic ulcer. The left subhepatic space is the lesser sac which communicates with the right through the foramen of Winslow. It may fill with fluid as a result of a perforation in the posterior wall of the stomach or from an inflamed or injured pancreas to form a pseudocyst of the pancreas.

Molecular Basis For The Side Effects Of Anticholinergics

The untoward effects associated with the use of anticholinergics are manifestations of their pharmacological actions, and usually occur on excessive dosage. The effects include dryness of mouth, blurred vision, difficulty in urination, increased intraocular tension, tachycardia, and constipation. Most of these side effects are lessened when the quaternary anticholinergics are administered orally in the treatment of peptic ulcer because of low absorption into the systemic circulation. In the case of tertiary amines the central side effects

Hiatal Hernia And Gastroesophageal Reflux

Diaphragm Crura

Medical management includes the following H2 blockers, antacids, and abstinence from alcohol and smoking (i.e. these are all the same medical management maneuvers used for peptic ulcer disease). In addition, the patient should sleep in an upright position, i.e. by placing shock blocks at the head of the bed. If the patient's symptoms have not resolved in 6 weeks, surgery may be indicated. This may be of several different types, the most commonly being a Nissen fundoplication.

Acid Secretion Bythe Stomach

On average, patients with duodenal ulcer produce about twice as much HC1 as normal subjects, but there is much overlap, and about half the patients with duodenal ulcer have acid outputs in the normal range. Patients with gastric ulcer produce normal or reduced amounts of acid.

Helicobacter Pylori Eradication

Colonisation of the stomach with Helicobacter pylori is seen in virtually all patients with duodenal ulcer and 70-80 of those with gastric ulcers 2 this close association is not seen in ulcers complicating NSAID therapy. In patients with duodenal ulcer there is an associated antral gastritis whereas with gastric ulcer, gastritis is more diffuse throughout the stomach. It is not known how Helicobacter pylori predisposes to peptic ulceration, but chronic infection with the organism, which establishes itself within and below the mucus layer, is associated with hypergastrinaemia and hyperacidity. The hypergastrinaemia may result from reduced antral production of somatostatin, which inhibits gastrin formation. Production of ammonia by urease by Helicobacter pylori may also play a role. With more extensive gastritis there is a reduction in parietal cell mass and decreased acid secretion. Although all patients colonised with Helicobacter pylori develop gastritis, only about 20 have ulcers or...

Therapeutic Uses Of Anticholinergics

The chief use of most of the antispasmodic agents is as an adjunct in the management of the peptic ulcer this group of drugs includes adiphenine, aminopentamide, amprotropine, dibutoline, diphemanil, glycopyrrolate, hexo-cyclium, homoatropine methylbromide, meth-scopolamine bromide, methscopolamine nitrate,

Test Methodology 1010 Lipase

Lipase enzymes catalyze the hydrolysis of glycerol esters of long- chain fatty acids. Lipase hydrolyzes dietary triacylglycerol at the ester bonds at carbons 1 and 3 of the molecule to produce monoacylglycerols and fatty acids. Lipase acts at the interface between water and lipid, or substrate therefore, the substrate must be in an emulsion, such at that found in association with bile salts. A cofactor, called colipase, is required for the reaction. Lipase is produced by the pancreas. Small amounts of lipase are also found in small intestine and stomach. The finding of increased concentrations of lipase in body fluids is clinically significant to the diagnosis of pancreatitis. Hyperlipemia is also found in nonpancreatic disorders, such as perforated peptic ulcers and intestinal obstruction.

Joseph B Muhlestein MD

Chronic infection has been found to be significantly associated with the development of atherosclerosis and the clinical complications of unstable angina, myocardial infarction, and stroke. A variety of infectious agents have been proposed to be involved in atherothrombosis, and, indeed, the number of implicated agents continues to increase each year. These include specific bacterial and viral agents, as well as a variety of agents associated with periodontal disease. However, failure to confirm initial reports of serological associations also has been common. The infectious agents with the most evidence to support an etiological role in atherosclerosis include Chlamydia pneumoniae and cytomegalovirus. In addition, evidence is mounting for a variety of other potential agents including other herpes viruses, influenza, other specific bacteria (such as Mycoplasma pneumoniae), and chronic infections with common bacterial agents (e.g., periodontal disease, chronic bronchitis, chronic...

Activity Efficacy and Safety of Corticosteroids in Palliative Treatment of Cancer Cachexia

Trial of Moertel et al. dates back to 1974 85 , and other important trials were published in the 1980s 86-89 , some considerations can be made approaching the results from an outcome point of view. All trials showed that corticosteroids (dex-amethasone or prednisolone, or methylpred-nisolone) induce a temporary benefit against different cachexia-related symptoms, improving the appetite, food intake, sensation of well-being, and performance status. Conversely, no trial demonstrated an improvement in body weight. Moreover, the trials of Robustelli della Cuna and Popiela 88, 89 approached the dimension of quality-of-life assessment during the treatment, and tried to go beyond symptom assessment in the outcome assessment in palliative care. Besides these interesting results detailed in Table 2, there is much evidence that corticosteroids can act against some other symptoms, that are related to, but not constitutive of, cancer cachexia, such as asthenia, or nausea and vomiting 90-93 . It...

Pathology of the Pancreas

Pancreatic endocrine tumors do occur, although less frequently than ductal or acinar tumors. Occasionally insulinomas, or insulin-secreting tumors, occur, most frequently in the body and tail of the pancreas instead of the head. Most of these are adenomas, benign secreting tumors. Non-beta islet cell tumors are associated with excessive secretion of gastrin or secretin. Hypergastrinemia serves as a diagnostic indicator and also causes the complication of peptic ulcers and other clinical findings associated with Zollinger-Ellison syndrome. Hypersecretion of secretin by these tumors is associated with watery diarrhea, hypokalemia, and achlorhydria without excessive gastrin secretion or peptic ulcers. Vasoactive intestinal peptide (VIP) carcinoma, sometimes called VIPoma, is rare. VIPomas secrete excessive amounts of VIP that causes a special clinical syndrome characterized by secretory diarrhea, hypokalemia, and achlorhydria.43

Ion Channels Regulating Sensory Nerve Excitability Conduction And Transmission Sensory Neuron Specific Na1 Channels

Voltage-gated Na+ channels, composed of one pore-forming a-subunit and one or more auxiliary p-subunits, are crucial for neuronal excitability and propagation of action potentials (178,179). Among the 10 known a-subunits are two tetrodotoxin-resistant Na+ channels, Nav1.8 (previously termed SNS PN3) and Nav1.9 (SNS2 NaN) and one tetrodotoxin-sensitive Na+ channel, Nav1.7 (PN1), that are preferentially expressed by nociceptive DRG neurons (178182). Tetrodotoxin-resistant Na+ currents are also present in vagal and spinal afferent neurons supplying the rat stomach (183) and in DRG neurons projecting to the rat ileum and colon (127,184-186). There is mounting evidence that tetrodotoxin-resistant Na+ channels play a role in neuropathic and inflammatory hyperalgesia (178,179). Experimental gastritis and trinitroben-zene sulphonic acid (TNBSA)-induced ileitis enhance the excitability of DRG neurons predominantly via an increase of Nav1.8 currents (183,186,187). Similar alterations in vagal...

Contributions To Neuronal Atrophy And Cell Death

Some studies suggest that stress and GCs may lead to neuronal death, but this conclusion is not without controversy. In rodents, chronic injection of exogenous stress levels of corticosterone in young rats produced neuronal loss of CA3 comparable to that seen in aged rats 19 , but it has also been shown that this effect is observed only if treatment begins when the rats are juveniles and does not happen if prolonged corticosterone exposure occurs only during adulthood 122 . Thus, high levels of corticosterone do not always cause neuron loss. Stress is even less likely to produce overt neuronal death than GC exposure 123 . Only truly exceptional levels of stress have ever been shown to cause neuron loss in the brain. Wild-born monkeys that died in captivity exhibiting multiple signs of severe social subordination stress (gastric ulcers, bite wounds, increased adrenal weight) have been shown to have stress-related changes in hippocampal neurons. These monkeys showed reduced numbers of...

TABLE 91 Abdominal Pain

Peptic Ulcer and Peptic ulcer refers to a demonstrable ulcer, usually in the duodenum or stomach. Dyspepsia causes similar more likely than gastric ulcer or The history of pain is typically Often food shorter than in peptic ulcer. The pain is persistent and slowly progressive. Food and antacids may bring relief, but not necessarily in any of these disorders and least commonly in gastric ulcer. Nausea, vomiting, belching, bloating heartburn (more common in duodenal ulcer) weight loss (more common in gastric ulcer). Dyspepsia is more common in the young (20-29 yr), gastric ulcer in those over 50 yr, and duodenal ulcer in those from 30-60 yr.

H2 receptor antagonists

These drugs bind selectively and competitively to the histamine H2 receptor on the basolateral membrane of the parietal cell. As well as inhibiting gastric acid release from histamine they inhibit acetylcholine- and gastrin-mediated acid secretion. This inhibitory effect can be overcome, particularly when gastrin levels are high, as occurs postprandially. In addition, tolerance may develop, probably as a result of down-regulation of receptors. Peptic ulcer healing with H2 receptor antagonists correlates best with suppression of nocturnal acid secretion and these drugs are often given in a single evening dose. The usual ulcer-healing course is 8 weeks.

CAIs In The Alimentary Tract

Regulation of the acid-base balance in the alimentary tract is a physiological process involving a number of proteins, such as ion transport proteins, plasma membrane receptors and their ligands and CAs. Even though, or maybe because, several CA isozymes are involved in this process, applicability of CAIs has been so far limited in the gastrointestinal tract. Most attractive have been speculations that CAIs can be useful for the therapy of peptic ulcers. This was an early approach to attack the machinery of the acid-producing cell by acetazolamide (Baron 2000). In 1939, Davenport suggested that CA might be essential for acid production, and, consequently, an inhibitor of this enzyme would inhibit gastric acid secretion. A few years later, Davenport (1946) retracted this theory, because early inhibitors such as sulfanilamide failed to inhibit gastric acid secretion. Janowitz et al. (1952, 1957) demonstrated marked but very brief acid inhibition by acetazolamide and concluded that its...

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.

Test Methodology 109 Amylase

Amylase is a hydrolase that catalyzes the breakdown of starch, glycogen, and some oligosaccharides. Calcium is a necessary cofactor in the reaction. Animal amylases, called alpha amylases, break down the alpha-1,4 glycosidic linkages in these substrates, producing glucose, maltose, and dextrins, which contain the branched products of degradation. Amylase is produced in the pancreas and salivary glands. Small amounts of amylase are also found in the small intestine and skeletal muscle. The finding of increased concentrations of amylase in blood and urine is clinically significant to the diagnosis of pancreatitis. Hyperamylasemia is also found in nonpancreatic disorders such as salivary gland tumor, mumps, perforated peptic ulcer, renal insufficiency, and diabetic ketoacidosis. Low levels of serum amylase may indicate pancreatic insufficiency such as found in cystic fibrosis.

Helicobacter Pylori H Pylori

Most patients with peptic ulcer disease are infected with H. pylori. Because ulcers recur in patients who have undergone successful H. pylori, eradication therapy, infection may not always be causative for the disease. Less than 5 of ulcer patients are H. pylori negative and in H. pylori positive patients only 10 of ulcers recur after eradicating the infection. Likely causes of ulcer recurrence are considered to be reinfection, the use of ulcerogenic drugs, and persistent gastric hypersecretion. However, true reinfection is rare and it is mcre likely that the most common cause of H. pylori recurrence is attributed to inadequate eradication. The significant reduction in H. pylori density produced by a combination of antibiotic and antisecretory therapy may reduce the levels of infection to below detectable levels (22). Rapid urease tests for H. pylori have a sensitivity of only 80-90 . Therefore histological examination is also used to con-fhm an initial noninvasive test result. Whole...

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...

Clinical Correlation

The fecal occult blood test measures hidden blood in feces. When visible blood is present in feces, it is not referred to as occult blood since it is not hidden. Occult blood is detected by a colori-metric test in which the peroxidase activity of the blood hemoglobin reacts with guaiac reagents to form a color. Occult blood is one of the most common tests for detecting a bleeding ulcer or malignancy in the gastrointestinal tract. Fecal occult blood also could result from trace amounts of blood excreted from hemorrhoids.

Diagnosis And Staging Of Gastric Malt Lymphoma

The most common presenting symptoms of gastric MALT lymphoma are dyspepsia, epigastric pain, nausea, and chronic manifestations of GI bleeding, such as anemia. The upper GI complaints often lead to an endoscopy that usually reveals nonspecific gastritis or peptic ulcer with mass lesions being unusual.41


Right upper abdominal pain of acute onset that occurs after ingestion of a fatty meal and is associated with nausea and vomiting is most suggestive of biliary colic as a result of gallstones. Duodenal ulcer pain is likely to be diminished with food, and gastric ulcer pain is not likely to have acute severe onset. Acute hepatitis is more likely to produce dull ache and tenderness.

What Is Pain

The International Association for the Study of Pain (IASP) has defined pain as an unpleasant sensory and emotional experience associated with noxious stimuli or described in such terms (1). Implicit in this definition are two important features of pain. First and foremost is that pain is a perception that occurs in a conscious brain, requiring activation of multiple cortical areas to produce an experience. In contrast, nociception is the term used to describe activity in either the peripheral or the central nervous system (CNS) evoked by noxious stimuli. Importantly, nociception may or may not result in the perception of pain. The implication of this distinction is that pain not only requires consciousness, but also an intact nervous system and a nervous system that has developed sufficiently such that activity in subcortical nocicep-tive circuits is able to influence activity in the appropriate cortical circuits (2). Second, pain has both sensory and emotional content. This notion is...

The Stomach

Gastric pain is most often modeled using distension, chemical challenge, or both, of the stomach. Many different chemicals have been used to produce gastric damage, the most common of these employed in animal models of visceral sensory transduction being hydrochloric acid or acetic acid. Intragastric administration (using a feeding tube) of hydrochloric acid, at a concentration that will induce c-fos expression in the brainstem (0.5 M), causes writhing movements indicative of a noxious visceral insult with a peak response approximately 45 minutes after administration (18). Even so, only 42 (15 of 36) of rats that received the acid infusion responded in this way (a figure reported to be similar to the incidence of pain produced in humans following infusion of hydrochloric acid onto symptomatic peptic ulcers). Following the publication of methods by which acetic acid could be used to produce gastric ulceration (19,20) came the development of the kissing ulcer'' (21,22). This ulceration...


The involvement of more than one endocrine hormone and neurotransmitter in the control of gastric acid secretion has resulted in a number of therapeutic approaches directed toward achieving its inhibition. Of these strategies both muscarinic and histamine H2-receptor antagonists have been used, with the latter being the method of choice for the control of acid-related disorders, particularly peptic ulcer disease, until the late 1980s. Along with the successful treatment of many patients

Helicobacter Pylori

Over the past decade or so H. pylori has been shown to play a causative role in gastric inflammation and peptic ulcer disease. Its role has been established because the presence of infection is a risk factor for the development of ulcers ulcers do not develop in the absence of infection, except when other known etiological factors exist, such as the use of nonsteroidal anti-inflammatory drugs care of the infection results in a dramatic drop in the rate of ulcer relapse, from 80 to 15 in the first year, with even lower rates thereafter and experimental infection of gerbils and mice causes gastroduodenal injury. Gastric infection with H. pylori is also found to be associated with the development of stomach cancer.

Diet Gallstones

Fig. 5.4 Vitamin A as adjunctive therapy in gastric ulcer. 56 men with chronic gastric ulcers were given standard antacid therapy (in doses necessary to reduce stomach pain) or antacid therapy plus 150 000 IU day vitamin A for 4 weeks. Ulcer sizes, which did not differ between groups at the beginning of treatment, were reduced in both groups, but healing was significantly greater in the vitamin A group. Complete healing of ulcers occurred in 19 of men treated with antacids alone, compared with 39 from the antacids plus vitamin A group. (Adapted from Patty I, etal. Lancet. 1982 2 876) Fig. 5.4 Vitamin A as adjunctive therapy in gastric ulcer. 56 men with chronic gastric ulcers were given standard antacid therapy (in doses necessary to reduce stomach pain) or antacid therapy plus 150 000 IU day vitamin A for 4 weeks. Ulcer sizes, which did not differ between groups at the beginning of treatment, were reduced in both groups, but healing was significantly greater in the vitamin A group....

Ulcer Disease

Peptic ulcers arise because of an imbalance of acid-secretory mechanisms and mucosal-pro-tective factors, and the rationale for their treatment is aimed at restoring that balance. The loss of balance between acid secretion and mucosal-protective factors varies among peptic ulcer types. In type I ulcers, which occur high in the stomach, acid hypersecretion is not necessarily evident, suggesting the importance of impaired mucosal-protective factors in this clinical setting. Type II ulcers, in contrast, include gastric ulcers, distal antral (prepyloric) ulcers, and duodenal ulcers. They are associated with acid hypersecretion and the impaired negative feedback effects of acidification on gastrin release and on continued acid secretion. The causes of gastric ulcers include H. pylori infection, nonsteroidal anti-inflammatory drugs (NSAIDs), environmental factors, and malignancy. Duodenal ulcers can result from hypersecretion of gastrin, which is assessed by evaluating fasting gastrin...

Management Of Gord

H2-receptor antagonists in conventional peptic ulcer healing doses are useful in the short-term management of mild oesophagitis but are less effective in the longer term and on maintenance treatment only one-third of patients will be in remission. Proton pump inhibitors are currently the most effective drugs. Conventional ulcer healing doses rapidly relieve reflux symptoms and heal oesophagitis in the majority of patients. Sometimes higher doses are needed, particularly for maintenance therapy. Over three-quarters of patients will still be in remission after 12 months' treatment with a proton pump inhibitor.

The Small Intestine

Tunel Short Bowel Syndrome Rats

Figure 2 Acetic acid produces gastric ulcers in the rat. Kissing ulcers (A), induced in a rat three days after intraluminal application of 60 acetic acid. Arrows indicate round ulcers on the posterior and anterior walls. Using a different method (injection of 20 acetic acid into the stomach wall), the visceromotor response to gastric distension is significantly enhanced from three days (B) to 60 days (C) after acetic acid treatment (p 0.05). Source (A) From Ref. 22 (B) Redrawn and adapted from Ref. 24. Figure 2 Acetic acid produces gastric ulcers in the rat. Kissing ulcers (A), induced in a rat three days after intraluminal application of 60 acetic acid. Arrows indicate round ulcers on the posterior and anterior walls. Using a different method (injection of 20 acetic acid into the stomach wall), the visceromotor response to gastric distension is significantly enhanced from three days (B) to 60 days (C) after acetic acid treatment (p 0.05). Source (A) From Ref. 22 (B) Redrawn and...

Treatment of AAION

Elderly patients with arteritic disease have a high level of sensitivity to the side effects of these drugs. Particularly important in the initiation of treatment with high-dose corticosteroids is the unpredictable complication of acute psychosis, which can be potentially life threatening. It is a good practice to admit patients to hospital for at least the first 24 h of therapy, so that a complication of this sort will be noticed. Routine testing of the blood levels of glucose and electrolytes is always indicated. Prophylaxis for the prevention of osteoporosis and or gastric ulcer is always indicated as well. It is difficult to say for how long these precautions should be maintained. Recurrent disease more than 6 months after the initial diagnosis is rare, though possible. There have not been many reports of patients losing vision at these later stages of treatment. Any recurrence of ischemic neuropathy would be difficult to differentiate from the nonarteritic form. There is always a...

Perioperative Pain

The principles of cancer pain management are now well established. The Cancer Pain Relief Program of the World Health Organization developed an analgesic ladder for the management of pain of increasing intensity (103). For mild pain, the recommendations start with NSAIDs. This drug class must be used with caution in those patients receiving steroids as part of their oncological management. NSAIDs are also contraindicated for patients who have renal insufficiency, intravascular volume depletion as seen with intractable vomiting, congestive heart failure, or peptic ulcer disease. A ceiling effect may occur, and increasing doses will lead to side effects without additional benefits. Unlike NSAIDs, opioids have no ceiling effect.


Assuming that the initial work-up for cardiac and pulmonary causes is negative and that the hemoglobin and hematocrit levels are low, a thorough evaluation for the cause of the anemia is necessary. A CBC with peripheral smear, reticulocyte count, iron study, vitamin Bp and folic acid levels would provide clues to the type of anemia that this patient has. A gastroenterology consult for possible EGD and colonoscopy to further investigate the source of gastrointestinal bleeding should be considered. The presence of epigastric and LUQ pain, along with long-term use of nonsteroidal antiinflammatory drugs (NSAlDs), should also raise a Hag for testing to rule out a bleeding ulcer.

Therapeutic Market

The therapy for gastric acid-related gastrointestinal disorders has evolved from nonspecific gastro-protective agents to treatments directed at specific sites regulating the secretion of gastric acid. H2-receptor antagonists and PPIs are currently the major therapies used to inhibit the production of gastric acid. The discovery that H. pylori infection was highly correlated with the presence of duodenal ulcer and hypersecretion of gastric acid has introduced an additional therapy that targets the eradication of H. pylori. This combination therapy of an antisecretory agent and an antibiotic has been shown to dramatically reduce the number of patients in which ulcer formation recurs (1).The incidence of upper gastrointestinal disorders such as ulcer and GERD shows an element of global variation. For example, in Western countries duodenal ulcers are more common, whereas in Eastern countries gastric ulcers predominate (2).These dif- i ferences may be attributable to any of a number of...


The previous section summarized the proportion of people who have symptoms of dyspepsia. However, these studies have not subjected these people to a diagnostic evaluation in order to determine whether or not they had functional dyspepsia. Many of these authors have, in fact, assumed that the majority of these people have functional dyspepsia. When determining the prevalence of functional dyspepsia, the investigators often exclude people who report a history of peptic ulcer disease, and approximately 8 of the population will report such a history (3,23). However, most people have not had any investigations and some people may report a history of peptic ulcer without having had any testing. Obviously, the absence of evaluation makes it very difficult to get a true estimate of the prevalence of functional dyspepsia. Still, the few studies that have evaluated people with dyspepsia in the community have not identified significant disease (24,29,30).

Adverse Reactions

Gastric and intestinal mucosal damage is the commonest adverse effect of NSAIDs. The physiological function of mucosal prostaglandins is cytoprotective, by inhibiting acid secretion, by promoting the secretion of mucus and by strengthening resistance of the mucosal barrier to back-diffusion of acid from the gastric lumen into the submucosal tissues where it causes damage. Inhibition of prostaglandin biosynthesis removes this protection. Indigestion, gastro-oesophageal reflux, erosions, peptic ulcer, gastrointestinal haemorrhage and perforation, and small and large bowel ulceration occur. In the UK an estimated 12 000 peptic ulcer complications and 1200 deaths per year are attributable to NSAID use.3 Toxicity relates to anti- Clinical trial evidence in general appears to support the theory that COX-2 selective inhibitors are as effective as, but have fewer adverse effects than, non-COX-2 selective compounds for example meloxicam is better tolerated than diclofenac or piroxicam.5-6 The...

Types Of Pain

Transmitted principally by fast conducting A-delta fibres (but to a lesser extent involves slow conducting type C fibres) and has major nociceptive input (physical trauma, pleurisy, myocardial infarct, perforated peptic ulcer). Patients perceive it as a transient, though sometimes severe threat and they react accordingly. It is a symptom that may be dealt with unhesitatingly and effectively with drugs, by injection if necessary, at the same time as the causative disease is addressed. The accompanying anxiety will vary according to the severity of the pain, and particularly according to its meaning for the patient, whether termination with recovery will soon occur, major surgery is threatened, or there is prospect of death or invalidism. The choice of drug will depend on the clinician's assessment of these factors. Morphine by injection has retained a preeminent place for over 100 years because it has highly effective antinociceptive and anti-anxiety effects modern opioids have not...