1

CMR COLLEGE OF PHARMACY

(Approved by AICTE & PCI)(Affiliated to JNTU)

(Kandlakoya, Medchal)

This is to certify that this is a bonafide record of the seminar entitled “PEPTIC ULCERS” carried out by CH.SIVA DEEPTHI (10t21s0116) During the academic year 2010-11 for partial fulfillment in degree of Master of pharmacy, Jawaharlal Nehru Technological University, Hyderabad.

PROF. K. RAJESHWAR DUTT Mr.J.ANUP

PRINCIPAL . Asst. Proffessor.

2

A seminar

On

“PEPTIC ULCERS”

Submitted to JNTU, Hyderabad.

In partial fulfillment for the award of the degree of Master of pharmacy.

PRESENTED BY

CH.SIVA DEEPTHI

(10t21s0116)

Under the guidance of

Mr.J.ANUP

Asst. Professor.

CMR COLLEGE OF PHARMACYKandlakoya, Medchal.

3

CONTENTS

INTRODUCTION

4

HISTORY

6

CLASSIFICATION 7

PHYSIOLOGY

8

SYMPTOMS

10

CAUSES

15

4

DIAGNOSIS

19

DRUGS

24

TREATMENT

36

HOME REMEDIES

40

PREVENTION

42

CONCLUSION

44

REFERENCE

45

5

INTRODUCTION

A stomach ulcer (also called a peptic ulcer) is a small erosion (hole) in the gastrointestinal tract. The most common type, duodenal, occurs in the first 12 inches of small intestine beyond the stomach. Ulcers that form in the stomach are called gastric ulcers. An ulcer is not contagious or cancerous. Duodenal ulcers are almost always benign, while stomach ulcers may become malignant.

Stomach ulcer disease is common, affecting millions of Americans yearly. The size of a stomach ulcer can range between 1/8 of an inch to 3/4 of an inch.

Find out more information about the stomach, or view it in relation to other organs in the body.

Ulcers are sores on the lining of your digestive tract. Your digestive tract consists of the esophagus, stomach, duodenum (the first part of the intestines) and intestines. Most ulcers are located in the duodenum. These ulcers are called duodenal ulcers. Ulcers located in the stomach are called gastric ulcers. Ulcers in the esophagus are called esophageal ulcers.

6

Most of us have heard of the term peptic ulcer. Stomach acid is what causes a peptic ulcer. Peptic ulcers can occur in the lower esophagus, stomach, or the duodenum. The most common of all are duodenum ulcers, followed by stomach ulcers. H. pylori is one of the major causes of peptic ulcers. The damage begins when the H. pylori bacterium starts to weaken and break the protective lining of the stomach. The soft tissue below this lining gets exposed and the strong stomach acid comes directly in contact with it. This acid keeps irritating the soft tissue and this constant irritation in time causes a bad sore / an ulcer.

A peptic ulcer, also known as PUD or peptic ulcer disease is an ulcer (defined as mucosal erosions equal to or greater than 0.5 cm) of an area of the gastrointestinal tract that is usually acidic and thus extremely painful. As many as 70-90% of ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach; however, only 40% of those cases go to a doctor. Ulcers can also be caused or worsened by drugs such as aspirin, Plavix (clopidogrel), ibuprofen, and other NSAIDs.

Contrary to general belief, more peptic ulcers arise in the duodenum (first part of the small intestine, just after the stomach) rather than in the stomach. About 4% of stomach ulcers are caused by a malignant tumor, so multiple biopsies are needed to exclude cancer. Duodenal ulcers are generally benign.

7

History.

John Lykoudis, a general practitioner in Greece, treated patients for peptic ulcer disease with antibiotics, beginning in 1958, long before it was commonly recognized that bacteria were a dominant cause for the disease.

Helicobacter pylori was rediscovered in 1982 by two Australian scientists, Robin Warren and Barry J. Marshall as a causative factor for ulcers. In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by colonization with this bacterium, not by stress or spicy food as had been assumed before. The H. pylori hypothesis was poorly received. so in an act of self-experimentation Marshall drank a Petri dish containing a culture of organisms extracted from a patient and five days later developed gastritis. His symptoms disappeared after two weeks, but he took antibiotics to kill the remaining bacteria at the urging of his wife, since halitosis is one of the symptoms of infection.[31] This experiment was published in 1984 in the Australian Medical Journal and is among the most cited articles from the journal.

In 1997, the Centers for Disease Control and Prevention, with other government agencies, academic institutions, and industry, launched a national education campaign to inform health care providers and consumers about the link between H. pylori and ulcers. This campaign reinforced the news that ulcers are a curable infection, and that health can be greatly improved and money saved by disseminating information about H. pylori.

8

In 2005, the Karolinska Institute in Stockholm awarded the Nobel Prize in Physiology or Medicine to Dr. Marshall and his long-time collaborator Dr. Warren "for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease". Professor Marshall continues research related to H. pylori and runs a molecular biology lab at UWA in Perth, Western Australia.

It was a previously widely accepted misunderstanding that the use of chewing gum resulted in gastric ulcers. The medical profession believed that this was because the action of masticating on gum caused the over-stimulation of the production of hydrochloric acid in the stomach. The low (acidic) pH (pH 2), or hyperchlorhydria was then believed to cause erosion of the stomach lining in the absence of food, thus causing the development of the gastric ulcers.

On the other hand, in the recent past, some believed that natural tree resin extract, mastic gum, actively eliminates the H. pylori bacteria. However, multiple subsequent studies have found no effect of using mastic gum on reducing H. pylori levels.

Modified Johnson Classification of peptic ulcers:

Type I: Ulcer along the body of the stomach, most often along the lesser curve at incisura angularis along the locus minoris resistentiae.

Type II: Ulcer in the body in combination with duodenal ulcers. Associated with acid over secretion.

Type III: In the pyloric channel within 3 cm of pylorus. Associated with acid oversecretion.

Type IV: Proximal gastroesophageal ulcer

Type V: Can occur throughout the stomach. Associated with chronic NSAID use (such as aspirin).

Classification

Stomach (called gastric ulcer) Duodenum (called duodenal ulcer)

Esophagus (called Esophageal ulcer)

9

Meckel's Diverticulum (called Meckel's Diverticulum ulcer With Pulpation is very tender.)

PHYSIOLOGY OF GASTRIC ACID SECRETION:

Gastric acid secretion is a complex, continuous process in which multiple central and peripheral factors contribute to a common endpoint: the secretion of H+ by parietal cells. Neuronal (acetylcholine, ACh), paracrine (histamine), and endocrine (gastrin) factors all regulate acid secretion .Their specific receptors (M3, H2, and CCK2 receptors, respectively) are on the basolateral membrane of parietal cells in the body and fundus of the stomach. The H2 receptor is a GPCR that activates the Gs-adenylylcyclase-cyclic AMP-PKA pathway. ACh and gastrin signal through GPCRs that couple to the Gq-PLC-IP3-Ca2+ pathway in parietal cells. In parietal cells, the cyclic AMP and the Ca2+-dependent pathways activate H+,K+-ATPase (the proton pump), which exchanges hydrogen and potassium ions across the parietal cell membrane. This pump generates the largest known ion gradient in vertebrates, with an intracellular pH of about 7.3 and an intracanalicular Ph of about0.8.

The most important structures for CNS stimulation of gastric acid secretion are the dorsal motor nucleus of the vagal nerve, the hypothalamus, and the solitary tract nucleus. Efferent fibers originating in the dorsal motor nuclei descend to the stomach via the vagus nerve and synapse with ganglion cells of the enteric nervous system. ACh release from postganglionic vagal fibers directly stimulates gastric acid secretion through muscarinic M3 receptors on the basolateral membrane of parietal cells. The CNS predominantly modulates the activity of the enteric nervous system via ACh, stimulating gastric acid secretion in response to the sight, smell, taste, or anticipation of food (the "cephalic" phase of acid secretion). ACh also indirectly affects parietal cells by increasing the release of histamine from the enterochromaffin-like (ECL) cells in the fundus of the stomach and of gastrin from Gcells in the gastric antrum. ECL cells, the source of gastric histamine secretion, usually are in close proximity to parietal cells. Histamine acts as a paracrine mediator, diffusing from its site of release to nearby parietal cells, where it activates H2 receptors. The critical role of histamine in gastric acid secretion is

10

dramatically demonstrated by the efficacy of H2-receptor antagonists in decreasing gastric acid secretion

Gastrin, which is produced by antral G cells, is the most potent inducer of acid secretion. Multiple pathways stimulate gastrin release, including CNS activation, local distention, and chemical components of the gastric contents. Gastrin stimulates acid secretion indirectly by inducing the release of histamine by ECL cells;a direct effect on parietal cells also plays a lesser role.

Somatostatin (SST), which is produced by antral D cells, inhibits gastric acid secretion. Acidification of the gastric luminal pH to <3 stimulates SST release, which in turn suppresses gastrin release in a negative feedback loop. SST-producing cells are decreased in patients with H. pylori infection, and the consequent reduction of SST's inhibitory effect may contribute to excess gastrin production.

Gastric Defenses Against Acid. The extremely high concentration of H+ in the gastric lumen requires robust defense mechanisms to protect the esophagus and the stomach. The primary esophageal defense is the lower esophageal sphincter, which prevents reflux of acidic gastric contents into the esophagus. The stomach protects itself from acid damage by a number of mechanisms that require adequate mucosal

11

blood flow, perhaps because of the high metabolic activity and oxygen requirements of the gastric mucosa. One key defense is the secretion of a mucus layer that protects gastric epithelial cells. Gastric mucus is soluble when secreted but quickly forms an insoluble gel that coats the mucosal surface of the stomach, slows ion diffusion, and prevents mucosal damage by macromolecules such as pepsin. Mucus production is stimulated by prostaglandins E2 and I2, which also directly inhibit gastric acid secretion by parietal cells. Thus, alcohol, aspirin, and other drugs that inhibit prostaglandin formation decrease mucus secretion and predispose to the development of acid-peptic disease. A second important part of the normal mucosal defense is the secretion of bicarbonate ions by superficial gastric epithelial cells. Bicarbonate neutralizes the acid in the region of the mucosal cells, thereby raising pH and preventing acid-mediated damage.

SIGNS AND SYMPTOMS:

Symptoms of a peptic ulcer can be

abdominal pain , classically epigastric with severity relating to mealtimes, after around 3 hours of taking a meal (duodenal ulcers are classically relieved by food, while gastric ulcers are exacerbated by it);

bloating and abdominal fullness;

waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus);

nausea, and copious vomiting;

loss of appetite and weight loss;

hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.

melena (tarry, foul-smelling feces due to oxidized iron from hemoglobin);

rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis. This is extremely painful and requires immediate surgery.

12

A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include NSAID (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase, and most glucocorticoids (e.g. dexamethasone and prednisolone).

In patients over 45 with more than two weeks of the above symptoms, the odds for peptic ulceration are high enough to warrant rapid investigation by EGD (see below).

The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, as gastric acid is secreted, or after the meal, as the alkaline duodenal contents reflux into the stomach. Symptoms of duodenal ulcers would manifest mostly before the meal—when acid (production stimulated by hunger) is passed into the duodenum. However, this is not a reliable sign in clinical practice.

Also, the symptoms of peptic ulcers may vary with the location of the ulcer and the patient's age. Furthermore, typical ulcers tend to heal and recur and as a result the pain may occur for few days and weeks and then wane or disappear. Usually,

13

children and the elderly do not develop any symptoms unless complications have arisen.

Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours commonly accompanies ulcers. This pain can be misinterpreted as hunger, indigestion or heartburn. Pain is usually caused by the ulcer but it may be aggravated by the stomach acid when it comes into contact with the ulcerated area. The pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it may last from few minutes to several hours and it may be worse when the stomach is empty. Also, sometimes the pain may flare at night and it can commonly be temporarily relived by eating foods that buffer stomach acid or by taking anti-acid medication. However, peptic ulcer disease symptoms may be different for every sufferer.

It is also important to remember that the symptoms listed below can occur as a result of other conditions, not just duodenal or gastric ulcers. These include gastro esophageal reflux disease (GERD), chronic dyspepsia without the presence of ulcers (often called non-ulcer or functional dyspepsia), gallbladder disease, liver disease and other disorders. Once again, if you are concerned about your symptoms, it is important that you see your doctor about your stomach problems.

common Symptoms of a Peptic Ulcer

The most common symptom of a peptic ulcer is a gnawing or burning pain in the

abdomen between the breastbone and navel. Duodenal ulcers typically cause

symptoms 2 to 5 hours after meals, when the stomach is empty, and can be relieved

by eating. Gastric ulcers, on the other hand, are classically made worse by eating.

You may experience pain soon after meals, and food won't improve symptoms. For

each, the duration of pain can be from a few minutes to a few hours.

Small ulcers may not cause any symptoms. Some ulcers can cause serious bleeding.

Abdominal pain is a common symptom but it doesn't always occur. The pain can differ a lot from person to person.

14

Feeling of fullness -- unable to drink as much fluid Hunger and an empty feeling in the stomach, often 1 - 3 hours after a meal

Mild nausea (vomiting may relieve symptom)

Pain or discomfort in the upper abdomen

Upper abdominal pain that wakes you up at night

Other possible symptoms include:

Bloody or dark tarry stools Chest pain

Fatigue

vomiting (if blood is in the vomit or the vomit looks like coffee grounds, which only happens with severe ulcers, call a doctor right away)

Weight loss

Anyone who thinks he or she may have an ulcer needs to see a doctor. Over time, untreated ulcers grow larger and deeper and can lead to other problems, such as bleeding in the digestive system or a hole in the wall of the stomach or duodenum, which can make someone very sick

Complications

Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery.

Perforation (a hole in the wall) often leads to catastrophic consequences. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain. Posterior wall perforation leads to pancreatitis; pain in this situation often radiates to the back.

15

Penetration is when the ulcer continues into adjacent organs such as the liver and pancreas.[6]

Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction. Patient often presents with severe vomiting.

Cancer is included in the differential diagnosis (elucidated by biopsy), Helicobacter pylori as the etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.

Warning signs that your ulcer is getting worse

You vomit blood. You vomit food eaten hours or days before.

You feel cold or clammy.

You feel unusually weak or dizzy.

You have blood in your stools (blood may make your stools look black or . . . like tar).

You have ongoing nausea or repeated vomiting.

16

You have sudden, severe pain.

You keep losing weight.

Your pain doesn't go away when you take your medicine.

Your pain reaches to your back

CAUSES:For almost 100 years, doctors believed that stress, spicy foods, and alcohol caused most ulcers. Now we know that most peptic ulcers are caused by a particular bacterial infection in the stomach and upper intestine, by certain medications, or by smoking.

In 1982, two doctors — Barry Marshall and Robin Warren — discovered a certain kind of bacteria that can live and grow in the stomach. Both doctors went on to win the Nobel Prize for their discovery. The medical name for these bacteria is Helicobacter pylori (or H. pylori, for short). Today doctors know that most peptic ulcers are caused by an infection from H. pylori.

Experts believe that 90% of all people with ulcers are infected with H. pylori. But strangely enough, most people infected with H. pylori don't develop an ulcer. Doctors aren't completely sure why, but think it may partly depend upon the individual person — for example, those who develop ulcers may already have a problem with the lining of their stomachs.

It's also thought that some people may naturally secrete more stomach acid than others — and it doesn't matter what stresses they're exposed to or what foods they eat. Peptic ulcers may have something to do with the combination of H. pylori infection and the level of acid in the stomach

17

As many as half of the world's population is infected with H. pylori. Those living in developing countries or crowded, unsanitary conditions are most likely to contract the bacterium, which is passed from person to person. H. pylori only grows in the stomach, and is usually contracted during childhood.

Interestingly, many people have this organism in their stomach, but don't get an ulcer or gastritis. Coffee drinking, smoking, and drinking alcohol increase your risk for an ulcer from H. Pylori

A major causative factor (60% of gastric and up to 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonizes the antral mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production by that part of the stomach, and gastrin secretion can either be decreased (most cases) resulting in hypo- or achlorhydria or increased. Gastrin stimulates the production of gastric acid by parietal cells and, in H. pylori colonization responses that increase gastrin, the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation.

Another major cause is the use of NSAIDs (see above). The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of

18

cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. COX-2 selective anti-inflammatories (such as celecoxib or the since withdrawn rofecoxib) preferentially inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration. As the prevalence of H. pylori-caused ulceration declines in the Western world due to increased medical treatment, a greater proportion of ulcers will be due to increasing NSAID use among individuals with pain syndromes as well as the growth of aging populations that develop arthritis.

The incidence of duodenal ulcers has dropped significantly during the last 30 years, while the incidence of gastric ulcers has shown a small increase, mainly caused by the widespread use of NSAIDs. The drop in incidence is considered to be a cohort-phenomenon independent of the progress in treatment of the disease. The cohort-phenomenon is probably explained by improved standards of living which has lowered the incidence of H. pylori infections.

Although some studies have found correlations between smoking and ulcer formation, others have been more specific in exploring the risks involved and have found that smoking by itself may not be much of a risk factor unless associated with H. pylori infection.Some suggested risk factors such as diet, spice consumption and blood type, were hypothesized as ulcerogens (helping cause ulcers) until late in the 20th century, but have been shown to be of relatively minor importance in the development of peptic ulcers. Similarly, while studies have found that alcohol consumption increases risk when associated with H. pylori infection, it does not seem to independently increase risk, and even when coupled with H. pylori infection, the increase is modest in comparison to the primary risk factor.

Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors, also cause multiple and difficult to heal ulcers.

19

Stress

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

An expert panel convened by the Academy of Behavioral Medicine Research concluded that ulcers are not purely an infectious disease and that psychological factors do play a significant role. Researchers are examining how stress might promote H. pylori infection. For example, Helicobacter pylori thrives in an acidic environment, and stress has been demonstrated to cause the production of excess stomach acid. This was supported by a study on mice showing that both long-term water-immersion-restraint stress and H. pylori infection were independently associated with the development of peptic ulcers.

A study of peptic ulcer patients in a Thai hospital showed that chronic stress was strongly associated with an increased risk of peptic ulcer, and a combination of chronic stress and irregular mealtimes was a significant risk factor.

Stomach ulcer statistics

1. About 20 million Americans develop at least one stomach ulcer during their lifetime.

2. Stomach ulcers affect about 4 million Americans every year.

3. More than 40,000 Americans have surgery because of persistent symptoms or problems from ulcers every year.

4. About 6,000 Americans die of stomach ulcer-related complications every year.

20

Risks of Developing a Stomach Ulcer

Family history of ulcers Smoking cigarettes or chewing tobacco

Drinking too much alcohol

Regular use of aspirin, ibuprofen, naproxen, or other nonsteroidal anti-inflammatory drugs (NSAIDs). Taking aspirin or NSAIDs once in awhile is safe for most people.

Zollinger-Ellison syndrome

Improper diet, irregular or skipped meals

Type O blood (for duodenal ulcers)

Stress does not cause an ulcer, but may be a contributing factor

Chronic disorders such as liver disease, emphysema, rheumatoid arthritis may increase vulnerability to ulcers

Being very ill, such as being on a breathing machine

Radiation treatments

Diagnosis:

Simple blood, breath, and stool tests can determine if you are infected with H. pylori. If you have symptoms, your doctor will determine if you should have these screening tests.

The most accurate way to diagnose H. pylori is through upper endoscopy of the esophagus, stomach, and duodenum. Because this procedure is invasive, it is generally only done on people suspected to have an ulcer, or who are at high risk for ulcers or other complications from H. pylori, such as stomach cancer.

21

Risk factors include being over 45 or having symptoms such as:

Anemia Difficulty swallowing

Gastrointestinal bleeding

Unexplained weight loss

The diagnosis is mainly established based on the characteristic symptoms. The stomach pain is usually the first to signal a peptic ulcer. In some cases, doctors may treat ulcers without diagnosing them with specific tests and observe if the symptoms resolve, meaning their primary diagnosis was accurate.

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

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

One of the reasons why blood tests are not reliable on establishing an accurate peptic ulcer diagnosis on their own is their inability to differentiate between past exposure to the bacteria and current infection. Additionally, a false-negative is possible with a blood test if the patient has recently been taking certain drugs, such as antibiotics or proton pump inhibitors.

22

Diagnosis of a stomach ulcerDiagnosing a stomach ulcer is done using a range of methods, including:

Endoscopy – a thin flexible tube is threaded down the oesophagus into the stomach under light anaesthesia. The endoscope is fitted with a small camera so the physician can see if there is an ulcer.

Barium meal – a chalky liquid is drunk and an x-ray is performed, showing the stomach lining. These tests are less common nowadays, but may be useful where endoscopy is unavailable.

Biopsy – a small tissue sample is taken during an endoscopy and tested in a laboratory. This biopsy should always be done if a gastric ulcer is found.

C14 breath test – to check for the presence of H. pylori. The bacteria convert urea into carbon dioxide. The test involves swallowing an amount of radioactive carbon (C14) and testing the air exhaled from the lungs. A non-radioactive test can be used for children and pregnant women.

23

The diagnosis of Helicobacter pylori can be made by:

Urea breath test (noninvasive and does not require EGD); Direct culture from an EGD biopsy specimen; this is difficult to do, and can

be expensive. Most labs are not set up to perform H. pylori cultures;

Direct detection of urease activity in a biopsy specimen by rapid urease test;

Measurement of antibody levels in blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy;

Stool antigen test;

Histological examination and staining of an EGD biopsy.

The breath test uses radioactive carbon atom to detect H. pylori. To perform this exam the patient will be asked to drink a tasteless liquid which contains the carbon as part of the substance that the bacteria breaks down. After an hour, the patient will be asked to blow into a bag that is sealed. If the patient is infected with H. pylori, the breath sample will contain radioactive carbon dioxide. This test provides the advantage of being able to monitor the response to treatment used to kill the bacteria.

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

Macroscopic appearance:

Gastric ulcers are most often localized on the lesser curvature of the stomach. The ulcer is a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and perpendicular borders. These borders are not elevated or irregular in the acute form of peptic ulcer, regular but with elevated borders and inflammatory surrounding in the chronic form. In the ulcerative form of gastric cancer the

24

borders are irregular. Surrounding mucosa may present radial folds, as a consequence of the parietal scarring.

Microscopic appearance

A gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and muscularis propria, produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.[19]

Differential diagnosis of epigastric pain

Peptic ulcer Gastritis

Stomach cancer

Gastroesophageal reflux disease

Pancreatitis

25

Hepatic congestion

Cholecystitis

Biliary colic

Inferior myocardial infarction

Referred pain (pleurisy, pericarditis)

Superior mesenteric artery syndrome

ANTIULCER DRUGS:

Antiulcer drugs are medicines used to treat ulcers in the stomach and the upper part of the small intestine.

The antiulcer drugs described here are used as part of the treatment for ulcers. Ulcers are sores or raw areas that form in the lining of the stomach or the duodenum (the upper part of the intestine). Those that form in the stomach are called gastric ulcers; in the duodenum, they are called duodenal ulcers. Both types are referred to as peptic ulcers. For a long time, physicians thought that stress and certain foods caused ulcers. Now they know that most ulcers are caused either by infection with a bacterium called Helicobacter pylori or by long-term use of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. In either case, something damages the barrier of mucus that normally protects the stomach and duodenum from the powerful acids and enzymes that the body produces to digest food. When that happens, the acids and enzymes begin to eat away at the unprotected tissue, causing ulcers.

Ulcers do not always cause symptoms. When they do, they usually cause a gnawing or burning pain -- something like hunger pangs -- between the breastbone and the navel. The pain often occurs early in the morning or between meals and may be temporarily relieved by eating or by taking antacids. Nausea, vomiting, loss of appetite and weight loss are other symptoms of ulcers. If ulcers bleed, the blood may show up in the form of black, tarry stools.

In addition to antibiotics to clear up the Helicobacter pylori infection, physicians use several types of antiulcer drugs that reduce the amount of acid the stomach produces or that protect the lining of the stomach and duodenum.

26

Getting the proper treatment for ulcers is important, because ulcers can lead to serious complications, such as bleeding, swelling, and scarring. If the swelling and scarring are severe, the opening between the stomach and intestine may become blocked. Untreated ulcers may also eat through the wall of the stomach or duodenum. When that happens, bacteria and partially digested food may leak into the body cavity and cause a life-threatening condition called peritonitis.

The three basic types of antiulcer drugs are H2-blockers, acid pump inhibitors, and mucosal protective medications. H2-blockers block the production of histamine, a substance that stimulates acid secretion. By blocking histamine, these drugs reduce the amount of acid the stomach produces. Examples of H2-blockers are cimetidine (Tagamet), famotidine (Pepcid), nizatidine (Axid) and ranitidine (Zantac). These drugs usually provide relief within a few days to a few weeks, depending on the severity of the ulcer. H2-blockers usually are given for 6-8 weeks to encourage healing. If the ulcers were caused by Helicobacter pylori, and the infection is not treated, the ulcers will usually recur and must be treated again. However, ulcers usually do not come back when the underlying infection is treated. Ulcers caused by nonsteroidal anti-inflammatory drugs do not need treatment with antibiotics.

Acid pump inhibitors completely block the production of stomach acid by stopping the final step in acid secretion. Omeprazole (Prilosec) is an acid pump inhibitor.

Mucosal protective medications create a protective barrier that allows the ulcer to heal and prevents further damage to the stomach and duodenum. Sucralfate (Carafate) is such a drug.

The proper dose depends on the type of antiulcer drug. Check with the physician who prescribed the drug or the pharmacist who filled the prescription for the correct dosage.

Always take antiulcer drugs exactly as directed. Never take larger or more frequent doses, and do not take the drug for longer than directed.

Although most of the drugs discussed here are available in both prescription and nonprescription (over-the-counter) forms, the nonprescription forms come in lower doses and are not intended for the treatment of ulcers. Anyone who has ulcers should be under a physician's care and should use the drugs and doses the physician prescribes.

27

Antiulcer drugs may mask the symptoms of stomach cancer. Anyone taking these drugs should make sure that his or her physician has ruled out the possibility of cancer.

Time may be needed for antiulcer medicines to relieve the pain. Be patient and keep taking the medicine as directed, even if it does not seem to be working at first. Antacids may be used to relieve the pain during this time, unless the physician says not to use them. If antacids and antiulcer drugs are taken together, allow half an hour to an hour between taking the antacid and taking the antiulcer drug.

Do not stop taking antiulcer drugs just because symptoms improve. Take the medicine for as long as the physician says to take it.

Smoking cigarettes may slow the healing of ulcers and make them more likely to develop again after treatment. Ideally, avoid smoking completely while taking antiulcer drugs or at least, avoid smoking after taking the last dose of the day will encourage healing of the ulcer.

Antiulcer drugs may affect the results of certain medical tests. Anyone who is taking antiulcer drugs should let the physician know before having skin tests for allergies or tests to find out how much acid the stomach produces.

Patients who are over 50 years old or who are severely ill may become temporarily confused while taking the antiulcer drugs called H2-blockers. These include cimetidine (Tagamet), famotidine (Pepcid), nizatidine (Axid), and ranitidine (Zantac). If this happens, notify the physician who prescribed the medicine. These drugs also increase the effects of alcohol, so anyone taking them should not drink alcoholic beverages without first checking with a physician or pharmacist. Large amounts of caffeine should also be avoided.

Patients who have phenylketonuria should be aware that Tagamet "Efferdose" tablets and granules contain phenylalanine.

Long-term use of the antiulcer drug omeprazole (Prilosec) can cause severe stomach inflammation.

People with certain medical conditions or who are taking certain other medicines can have problems if they take antiulcer drugs. Before taking these drugs, be sure to let the physician know about any of these conditions:

28

Anyone who has had unusual reactions to Axid, Pepcid, Prilosec, Tagamet, Zantac, or similar drugs in the past should let his or her physician know before taking antiulcer drugs. The physician should also be told about any allergies to foods, dyes, preservatives, or other substances.The effects of taking antiulcer drugs during pregnancy have not been fully studied. Women who are pregnant or plan to become pregnant should check with their physicians about whether to use antiulcer drugs.

Antiulcer drugs can pass into breast milk and may affect nursing babies. Women who are breastfeeding and need to take antiulcer drugs should check with their physicians. Not breastfeeding until treatment with the drugs is finished may be necessary.

Before using antiulcer drugs, people with any of these medical problems should make sure their physicians are aware of their conditions:

Kidney disease Liver disease

Weakened immune system

Obstruction of the gastrointestinal tract.

Taking antiulcer drugs with certain other drugs may affect the way the drugs work or may increase the chance of side effects.

The most common side effects are dizziness, drowsiness, gas, headache, indigestion, nausea, vomiting, abdominal or stomach pain, and inflammation of the nose. These problems usually go away as the body adjusts to the drug and do not require medical treatment. Less common side effects, such as blurred or dimmed vision, constipation, itching, rash, sleeplessness, abnormal dreams, breast swelling or tenderness, and backache also may occur and do not need medical attention unless they do not go away or they interfere with normal activities.

More serious side effects are not common, but may occur. If any of the following side effects occur, check with the physician who prescribed the medicine as soon as possible:

Confusion Fast, slow, pounding, or irregular heartbeat

29

Sore throat

Fever

Tightness in chest

Unusual bruising or bleeding

Unusual tiredness or weakness

Convulsions (seizures)

Drowsiness.

Other rare side effects may occur. Anyone who has unusual symptoms after taking antiulcer drugs should get in touch with his or her physician.

Antiulcer drugs may interact with a variety of other medicines. When this happens, the effects of one or both of the drugs may change or the risk of side effects may be greater. Anyone who takes antiulcer drugs should let the physician know all other medicines he or she is taking. Among the drugs that may interact with certain antiulcer drugs are:

Aspirin Alcohol Antacids such as Mylanta and Maalox Blood-thinning drugs such as warfarin (Coumadin) Other antiulcer drugs Iron Disulfiram (Antabuse) Cyclosporine (Sandimmune, Neoral) Antifungal drugs such as fluconazole (Diflucan) and ketoconazole (Nizoral) Medicines for irregular heartbeat such as amiodarone (Cordarone), tocainide (Tonocard), quinidine preparations such as Quinidex, and procainamide (Procan) Nicotine (in cigarettes or in smoking cessation drugs, such as Nicoderm and Nicorette).

Anti Ulcer Drugs are medicines used to treat ulcers in the stomach and the upper partofthesmallintestine.

Purpose:The Anti Ulcer Drugs are used as part of the treatment for ulcers. Ulcers are sores or raw areas that form in the lining of the stomach or the duodenum (the upper part of the intestine). Those that form in the stomach are called Gastric Ulcers; in the duodenum, they are called Duodenal Ulcers. Both types are referred to as Peptic

30

Ulcers. For a long time, physicians thought that stress and certain foods caused ulcers.

Now they know that most ulcers are caused either by infection with a bacterium called Helicobacter Pylori or by long-term use of aspirin or other Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), such as Ibuprofen. In either case, something damages the barrier of mucus that normally protects the stomach and duodenum from the powerful acids and enzymes that the body produces to digest food. When that happens, the acids and enzymes begin to eat away at the unprotected tissue ulcers.

1) H2 RECEPTOR ANTAGONISTNIZATIDINE

Nizatidine

FAMOTIDINE

31

Famotidine

CIMETIDINE

Cimetidine

RANITIDINE

Ranitidine

32

2) PROTON INHIBITORSOMEPRAZOLE

Omeprazole

33

3) PROTETIVE AGENTSSUCRALFATE

Sucralfate

MISOPROSTOL

Misoprostol

4) ANTIBIOTICS

34

AMOXICILLIN

Amoxicillin

COMMON SIDE EFFECTS.

Antiulcer Drugs

Brand Name(Generic Name)

Possible Common Side Effects Include:

Axid (nitzatidine) Diarrhea, headache, nausea and vomiting, sorethroat

Carafate (sucralfate) Constipation, insomnia, hives, upset stomach,vomiting

Cytotec (misoprostol) Cramps, diarrhea, nausea, gas, headache,menstrual disorders (including heavy bleedingand severe cramping)

Pepcid (famotidine) Constipation or diarrhea, dizziness, fatigue, fever

Prilosec (omeprazole)Nausea and vomiting, headache, diarrhea,abdominal pain

Tagamet (cimetidine) Headache, breast development in men, depres-sion and disorientation

35

Antiulcer Drugs

Brand Name(Generic Name)

Possible Common Side Effects Include:

Zantac(ranitidinehydrochloride)

Headache, constipation or diarrhea, joint pain

Description

The proton pump inhibitors block the secretion of gastric acid by the gastric parietal cells. The extent of inhibition of acid secretion is dose related. In some cases, gastric acid secretion is completely blocked for over 24 hours on a single dose. In addition to their role in treatment of gastric ulcers, the proton pump inhibitors are used to treat syndromes of excessive acid secretion (Zollinger-Ellison Syndrome) and gastroesophageal reflux disease (GERD).

Histamine H-2 receptor blockers stop the action of histamine on the gastric parietal cells, inhibiting the secretion of gastric acid. These drugs are less effective than the proton pump inhibitors, but may achieve a 75-79% reduction in acid secretion. Higher rates of acid inhibition may be achieved when the drug is administered by the intravenous route. The H-2 receptor blockers may also be used to treat heartburn and hypersecretory syndromes. When given before surgery, the H-2 receptor blockers are useful in prevention of aspiration pneumonia.

Sucralfate (Carafate), a substituted sugar molecule with no nutritional value, does not inhibit gastric acid, but rather, reacts with existing stomach acid to form a thick coating that covers the surface of an ulcer, protecting the open area from further damage. A secondary effect is to act as an inhibitor of the digestive enzyme pepsin. Sucralfate does not bind to the normal stomach lining. The drug has been used for prevention of stress ulcers, the type seen in patients exposed to physical stress such as burns and surgery. It has no systemic effects.

Recommended dosage

The doses of the proton pump inhibitors and H-2 receptor blockers vary depending on the drug and condition being treated. Consult individual references.

36

The dose of sucralfate for acute ulcer therapy is 1 gram four times a day. After the ulcer has healed, maintenance treatment may continue at 1 gram two times daily.

Precautions

The proton pump inhibitors are generally well tolerated, and the most common adverse effects are diarrhea, itching, skin rash, dizziness and headache. Muscle aches and a higher than normal rate of respiratory infections are among the other adverse reactions reported. Omeprazole has an increased rate of fetal deaths in animal studies. It is not known if these drugs are excreted in human milk, but because of reported adverse effects to infants in animal studies, it is recommended that proton pump inhibitors not be used by nursing mothers.

The H-2 receptor blockers vary widely in their adverse effects. Although they are generally well tolerated, cimetidine may cause confusion in elderly patients, and has an antiandrogenic effect that may cause sexual dysfunction in males. Famotidine has been reported to cause headache in 4.7% of patients. It is advisable that mothers not take H-2 receptor blockers while nursing.

Sucralfate is well tolerated. It is poorly absorbed, and its most common side effect is constipation in 2% of patients. Diarrhea, nausea, vomiting, gastric discomfort, indigestion, flatulence, dry mouth, rash, pruritus (itching), back pain, headache, dizziness, sleepiness, and vertigo have been reported, as well as rare allergic responses. Because sucralfate releases small amounts of aluminum into the system, it should be used with caution in patients with renal insufficiency. There is no information available about sucralfate's safety in breastfeeding.

Interactions

Proton pump inhibitors may increase the pH of the stomach. This will inactivate some antifungal drugs that require an acid medium for effectiveness, notable itraconazole and ketoconazole.

H-2 receptor blocking agents have a large number of drug interactions. Consult individualized references.

37

KEY TERMS

Hypersecretory— Excessive production of a bodily secretion. The most common hypersecretory syndrome of the stomach is Zollinger-Ellison Syndrome, a syndrome consisting of fulminating intractable peptic ulcers, gastric hypersecretion and hyperacidity, and the occurrence of gastrinomas of the pancreatic cells of the islets of Langerhans.

Inflammation— Pain, redness, swelling, and heat that usually develop in response to injury or illness.

Mucous— Thick fluid produced by the moist membranes that line many body cavities and structures.

Nonsteroidal anti-inflammatory drug (NSAID)— A type of medicine used to relieve pain, swelling, and other symptoms of inflammation, such as ibuprofen or ketoprofen.

Sucralfate should not be used with aluminum containing antacids, because of the risk of increased aluminum absorption. Sucralfate may inhibit absorption and reduce blood levels of anticoagulants, digoxin, quinidine, ketoconazole, quinolones and phenytoin.

Treatment:Ulcers caused by H. pylori bacteria are generally treated with a combination of medications:

← Usually two antibiotics to kill the H. pylori bacteria are taken every day for about 2 weeks.

← Antacids — acid blockers or proton pump inhibitors — are given for 2 months or longer to lessen the amount of acid in the stomach and help protect the lining of the stomach so the ulcer can heal.

38

Treatment involves a combination of medications to kill the H. pylori bacteria (if present), and reduce acid levels in the stomach. This strategy allows your ulcer to heal and reduces the chance it will come back.

Take all of your medications exactly as prescribed.

If you have a peptic ulcer with an H. pylori infection, the standard treatment uses different combinations of the following medications for 5 - 14 days:

Two different antibiotics to kill H. pylori, such as clarithromycin (Biaxin), amoxicillin, tetracycline, or metronidazole (Flagyl)

Proton pump inhibitors such as omeprazole (Prilosec), lansoprazole (Prevacid), or esomeprazole (Nexium)

Bismuth (the main ingredient in Pepto-Bismol) may be added to help kill the bacteria

If you have an ulcer without an H. pylori infection, or one that is caused by taking aspirin or NSAIDs, your doctor will likely prescribe a proton pump inhibitor for 8 weeks.

You may also be prescribed this type of medicine if you must continue taking aspirin or NSAIDs for other health conditions.

Other medications that may be used for ulcer symptoms or disease are:

Misoprostol, a drug that may help prevent ulcers in people who take NSAIDs on a regular basis

Medications that protect the tissue lining (such as sucralfate)

If a peptic ulcer bleeds a lot, an EGD may be needed to stop the bleeding. Surgery may be needed if bleeding cannot be stopped with an EGD,

The best way to stop any further growth of your stomach ulcer is to follow a healthy diet. It must contain non-acidic meals along with liquid meals. Sour agents like lemon should be strictly avoided in the diet. [20] Younger patients with ulcer-

39

like symptoms are often treated with antacids or H2 antagonists before EGD is undertaken. Bismuth compounds may actually reduce or even clear organisms, though the warning labels of some bismuth subsalicylate products indicate that the product should not be used by someone with an ulcer.

Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue (Misoprostol) in order to help prevent peptic ulcers, which may be a side-effect of the NSAIDs.

When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. Clarithromycin, Amoxicillin, Tetracycline, Metronidazole) and 1 proton pump inhibitor (PPI), sometimes together with a bismuth compound. In complicated, treatment-resistant cases, 3 antibiotics (e.g. amoxicillin + clarithromycin + metronidazole) may be used together with a PPI and sometimes with bismuth compound. An effective first-line therapy for uncomplicated cases would be Amoxicillin + Metronidazole + Pantoprazole (a PPI). In the absence of H. pylori, long-term higher dose PPIs are often used.

Treatment of H. pylori usually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics. Since the widespread use of PPI's in the 1990s, surgical procedures (like "highly selective vagotomy") for uncomplicated peptic ulcers became obsolete.

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

Ranitidine provides relief of peptic ulcers, heartburn, indigestion and excess stomach acid and prevention of these symptoms associated with excessive consumption of food and drink. Ranitidine is available over the counter from a pharmacy and works by decreasing the amount of acid the stomach produces allowing healing of ulcers. Zantac tablets contain Ranitidine 150mg as the active ingredient which can also be bought generically.

Balance diet:

40

Stress free life style, healthy food habit, balanced diet rich in food and vegetables are very important for keeping our body system healthy. Patient suffering from peptic ulcer should take diet rich in green leafy vegetable, fruits, milk, cheese, etc. However, they should never eat junk foods, oily and unhealthy foods. Drink lots of water, milk, etc., this too will keep the body temperature low and also controls acidity. However, do not add sugar to the milk.

Stressful life style is one of the root causes of several diseases. Patient suffering from peptic ulcer should live a stress-free life, should go for morning and evening walk, and do mild exercises, and yoga and meditations. Never eat in hurry, take food timely and full of nutrients, eat small meals 3-4 times a day, chew your food properly, all this will help in digestion of food, will prevent acidity and other diseases.

Diets for Stomach Ulcers

This diet is a guideline that may help to decrease gastric irritation and excessive gastric acid secretion. This diet may also help prevent uncomfortable side effects such as heartburn.

Eat three small meals and three snacks evenly spaced throughout the day. It is important to avoid periods of hunger or overeating.

Eat slowly and chew foods well.

Be relaxed at mealtime.

Sit up while eating and for 1 hour afterward.

Avoid eating within 3 hours before bedtime. Bedtime snacks can cause gastric acid secretion during the night.

Cut down on caffeine-containing foods and beverages, citrus and tomato products, and chocolate if these foods cause discomfort.

Include a good source of protein (milk, meat, egg, cheese, etc.) at each meal and snack.

Antacids should be taken in the prescribed dose, One-hour and 3 hours after meals and prior to bedtime. This regimen is most likely to keep the acidity of the stomach at the most stable and lowest level.

41

Milk and cream feedings should not be used as antacid therapy. Although milk protein has an initial neutralizing effect on gastric acid, it is also a very potent stimulator. Hourly feedings of milk have been shown to produce a lower pH than three regular meals.

Caffeine-containing beverages (coffee, tea, and cola drinks) and decaffeinated coffee cause increased gastric acid production but may be taken in moderation at or near mealtime, if tolerated.

Home Remedies for Peptic Ulcer

Given below are the simplest and the most effective home remedies for the treatment of peptic ulcers.

Fenugreek (methi) seeds:

42

Take 2-3 tablespoon of fenugreek (methi) seeds and boil it in a glass of water. Add little amount of soil to it. Allow the mixture to boil till it become half of its constituent. Take this mixture 2-3 times a day, until the ulcer is not cured completely. One of the useful home remedies for peptic ulcers.

Fruits:

Among various other fruits, banana is considered as one of an effective fruit for treating peptic ulcer. Banana helps in lowering the acidic substance inside the body. Take 2-3 bananas mixed in a glass of milk for 4-5 times a day.

Similarly, wood apple ( bael ) is also very useful. Take few bael leaves and keep it into water overnight. Drain the mixture and take this 2-3 times a day. This works great for peptic ulcer patient. One of the useful home remedies for peptic ulcers.

Milk:

Milk is really good for patient with peptic ulcer. Patient should take 2-3 glasses of water every day. Warm milk containing drops of castor oil is also very good for treating peptic ulcer.

Lemon:

Lemon extract or juice is also very effective in treating peptic ulcer. Prepare fresh lemon juice, add little amount of salt to it. This drink helps in digestion and hence helps in treating peptic ulcers. This is one of the best home remedies for peptic ulcers.

Vegetables:

Among vegetables cabbage is very useful for treating peptic ulcer. Cut cabbage into small pieces, allow the vegetable to boil in water till the constituent become half. Drain the mixture and take this 2-3 time a day. One can also add little amount of black pepper powder to it.

Drumsticks:

43

Drumstick leaves are also an effective home remedy for the treatment of peptic ulcer. Take 15-20 leaves of drumstick and make its paste. Mix this paste in fresh curd. Take this 2-3 times a day. This is one of the important home remedies for peptic ulcers.

Prevention:Doctors are not totally certain how H. pylori bacteria are transmitted from person to person. The bacteria have been found in saliva. They also may be spread through food, water, or contact with vomit (puke) that has been infected with the bacteria.

44

The best advice in ulcer prevention is to always wash your hands after you use the bathroom and before you eat and to take good care of your body by exercising regularly and not smoking or drinking.

Avoid aspirin, ibuprofen, naproxen, and other NSAIDs. Try acetaminophen instead. If you must take such medicines, talk to your doctor first. Your doctor may:

Test you for H. pylori first Have you take proton pump inhibitors (PPIs) or an acid blocker

Have you take a drug called Misoprostol

The following lifestyle changes may help prevent peptic ulcers:

Do not smoke or chew tobacco. Limit alcohol to no more than two drinks per day.

Cure:

If H. pylori is found to be the cause of the ulcer, you will be given drugs that will kill the bacteria, and at the same time will coat the ulcer and reduce the stomach acid to a minimum so that the ulcer can be cured. Most of these drugs will be antibiotics and the dosage would depend on the severity of the infection. If it is just the beginning of an ulcer the medication and dosage will be minimal, but if the ulcers have spread, the prescribed drugs will increase, causing unpleasant side effects. These side effects happen due to the antibiotics and can include a bad taste in the mouth leading to a loss of taste and appetite, vomiting, diarrhea, and headache. Treatment usually carries for 2 to 3 weeks. In most of the cases the patient will feel much better after this and will be cured fully within a couple of months with the right medication.

Whenever you notice any symptoms that may point towards a stomach ulcer, do not try to take medication on your own. Not even antacids. This may just worsen your condition. You must contact your doctor immediately and only take the prescribed drugs. This will ensure a fast and total recovery.

45

When you recognize any symptom, you must totally avoid alcohol, smoking, taking any sort of aspirin, and eating spicy food till you seek medical help and are totally cured. All of these will just aggravate and speed up the ulcer forming process.

CONCLUSION

H.Pylory is the mostly responsible for ulcers, Should avoid contamination.

Smoking and alcoholism should be controlled

46

Eating junk food shoud be avoided

Long term use of asprin and NSAIDS should be prevented.

Reference listFantry, G. T. (2005, May 6). Peptic Ulcer Disease. Retrieved September 4th, 2006, from www.emedicine.com/med/topic1776.htm

General Practice Notebook (2006). Peptic Ulcer. Retrieved September 10th, 2006, from www.gpnotebook.co.uk/simplepage.cfm?ID=630849536

47

Microbe Wiki (2006, August 16). Heliobacter. Retrieved September 10th, 2006, from www.microbewiki.kenyon.edu/index.php/Helicobacter

Moore, R. A. (1995). Helicobacter pylori and peptic ulcer: A systematic review of effectiveness and an overview of the economic benefits of implementing what is known to be effective. Oxford: Cortecs Limited and Health Technology Evaluation Association.

Pounder, R. (1994). Peptic ulceration. Medicine International, 22:6, 225-30.

Rodney, W.M. (2005, Summer). H. Pylori eradication options for peptic ulcer. Nurse Practitioners Prescribing Reference,12(2), 150.

Uphold, C. R. & Graham, M. V. (2003). Clinical Guidelines in Family Practice (4th ed.). Gainesville, FL: Barmarrae Books, Inc.

Black, J. Reflections on the analytical pharmacology of histamine H2-receptor antagonists.Gastroenterology, 1993, 105:963-968.PUBMED

Chong, E., and Ensom, M.H. Pharmacogenetics of the proton pump inhibitors: a systematic review. Pharmacotherapy, 2003, 23:460-471. PUBMED

Cook, D., Guyatt, G., Marshall, J., et al. Comparison of sucralfate and ranitidine for the prevention of upper gastrointestinal bleeding in patients requiring mechanical ventilation. Canadian Critical Care Trials Group. N. Engl. J. Med., 1998,  338:791-797. PUBMED

Dickson, E.J., and Stuart, R.C. Genetics of response to proton pump inhibitor therapy: clinical implications. Am. J. Pharmacogenomics, 2003, 3:303-315. PUBMED

Fackler, W.K., Ours, T.M., Vaezi, M.F., and Richter, J.E. Long-term effect of H2RA therapy on nocturnal gastric acid breakthrough. Gastroenterology, 2002, 122:625-632. PUBMED

Freston, J., Chiu, Y.L., Pan, W.J., Lukasik, N., and Taubel, J. Oral bioavailability of pantoprazole suspended in sodium bicarbonate solution. Am. J. Health Syst. Pharm., 2003,  60:1324-1329.

48

Graham, D.Y. Therapy of Helicobacter pylori: current status and issues. Gastroenterology, 2000, 118:S2-S8.

Howden, C.W., and Hunt, R.H. Guidelines for the management of Helicobacter pylori infection. Ad Hoc Committee on the Practice Parameters of the American College of Gastroenterology. Am. J. Gastroenterol., 1998,  93:2330-2338. PUBMED

Klinkenberg-Knol, E.C., Festen, H.P., Jansen, J.B., et al. Long-term treatment with omeprazole for refractory esophagitis: efficacy and safety. Ann. Intern. Med., 1994, 121:161-167. PUBMED

Kuipers, E.J., and Meuwissen, S.G. The efficacy and safety of long-term omeprazole treatment for gastroesophageal reflux disease. Gastroenterology, 2000, 118:795-798. PUBMED

Lanza, F.L. A guideline for the treatment and prevention of NSAID-induced ulcers. Members of the Ad Hoc Committee on Practice Parameters of the American College of Gastroenterology. Am. J. Gastroenterol., 1998,  93:2037-2046. PUBMED

Richter, J.E. Gastroesophageal reflux disease during pregnancy. Gastroenterol. Clin. North Am., 2003,  32:235-261. PUBMED

Rostom, A., Dube, C., Wells, G., et al. Prevention of NSAID-induced gastroduodenal ulcers. In, The Cochrane Library, Issue 2. John Wiley & Sons, Ltd., Chichester, UK, 2004.

Sandevik, A.K., Brenna, E., and Waldum, H.L. Review article: the pharmacological inhibition of gastric acid secretion-tolerance and rebound. Aliment. Pharmacol. Ther., 1997,  11:1013-1018.

Suerbaum, S., and Michetti, P. Helicobacter pylori infection. N. Engl. J. Med., 2002,  347:1175-1186. PUBMED

Wolfe, M.M., and Sachs, G. Acid suppression: optimizing therapy for gastroduodenal ulcer healing, gastroesophageal reflux disease, and stress-related erosive syndrome. Gastroenterology, 2000, 118:S9-S31.

49