peptic ulcer doc

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peptic ulcer doc

  1. 1. 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 partialfulfillment in degree of Master of pharmacy, Jawaharlal Nehru Technological University,Hyderabad.PROF. K. RAJESHWAR DUTT Mr.J.ANUP PRINCIPAL . Asst. Proffessor.
  2. 2. 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 PHARMACY Kandlakoya, Medchal.
  3. 3. 3CONTENTS INTRODUCTION 4 HISTORY 6 CLASSIFICATION 7 PHYSIOLOGY 8 SYMPTOMS 10 CAUSES 15 DIAGNOSIS 19 DRUGS 24 TREATMENT 36 HOME REMEDIES 40 PREVENTION 42 CONCLUSION 44 REFERENCE 45
  4. 4. 4INTRODUCTION A stomach ulcer (also called a peptic ulcer) is a small erosion(hole) in the gastrointestinal tract. The most common type, duodenal, occurs in thefirst 12 inches of small intestine beyond the stomach. Ulcers that form in thestomach are called gastric ulcers. An ulcer is not contagious or cancerous.Duodenal ulcers are almost always benign, while stomach ulcers may becomemalignant.Stomach ulcer disease is common, affecting millions of Americans yearly. The sizeof 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 organsin the body.Ulcers are sores on the lining of your digestive tract. Your digestive tract consistsof the esophagus, stomach, duodenum (the first part of the intestines) andintestines. Most ulcers are located in the duodenum. These ulcers are calledduodenal ulcers. Ulcers located in the stomach are called gastric ulcers. Ulcers inthe esophagus are called esophageal ulcers.
  5. 5. 5Most of us have heard of the term peptic ulcer. Stomach acid is what causes apeptic ulcer. Peptic ulcers can occur in the lower esophagus, stomach, or theduodenum. The most common of all are duodenum ulcers, followed by stomachulcers. H. pylori is one of the major causes of peptic ulcers. The damage beginswhen the H. pylori bacterium starts to weaken and break the protective lining ofthe stomach. The soft tissue below this lining gets exposed and the strong stomachacid comes directly in contact with it. This acid keeps irritating the soft tissue andthis 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 asmucosal erosions equal to or greater than 0.5 cm) of an area of the gastrointestinaltract that is usually acidic and thus extremely painful. As many as 70-90% ofulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that livesin the acidic environment of the stomach; however, only 40% of those cases go toa 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 ofthe small intestine, just after the stomach) rather than in the stomach. About 4% ofstomach ulcers are caused by a malignant tumor, so multiple biopsies are needed toexclude cancer. Duodenal ulcers are generally benign.
  6. 6. 6History.John Lykoudis, a general practitioner in Greece, treated patients for peptic ulcerdisease with antibiotics, beginning in 1958, long before it was commonlyrecognized that bacteria were a dominant cause for the disease.Helicobacter pylori was rediscovered in 1982 by two Australian scientists, RobinWarren and Barry J. Marshall as a causative factor for ulcers. In their originalpaper, Warren and Marshall contended that most stomach ulcers and gastritis werecaused by colonization with this bacterium, not by stress or spicy food as had beenassumed before. The H. pylori hypothesis was poorly received. so in an act of self-experimentation Marshall drank a Petri dish containing a culture of organismsextracted from a patient and five days later developed gastritis. His symptomsdisappeared after two weeks, but he took antibiotics to kill the remaining bacteriaat the urging of his wife, since halitosis is one of the symptoms of infection.[31] Thisexperiment was published in 1984 in the Australian Medical Journal and is amongthe most cited articles from the journal.In 1997, the Centers for Disease Control and Prevention, with other governmentagencies, academic institutions, and industry, launched a national educationcampaign to inform health care providers and consumers about the link between H.pylori and ulcers. This campaign reinforced the news that ulcers are a curableinfection, and that health can be greatly improved and money saved bydisseminating information about H. pylori.
  7. 7. 7In 2005, the Karolinska Institute in Stockholm awarded the Nobel Prize inPhysiology or Medicine to Dr. Marshall and his long-time collaborator Dr. Warren"for their discovery of the bacterium Helicobacter pylori and its role in gastritisand 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 gumresulted in gastric ulcers. The medical profession believed that this was because theaction of masticating on gum caused the over-stimulation of the production ofhydrochloric acid in the stomach. The low (acidic) pH (pH 2), or hyperchlorhydriawas 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, multiplesubsequent studies have found no effect of using mastic gum on reducing H. pylorilevels.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) • Meckels Diverticulum (called Meckels Diverticulum ulcer With Pulpation is very tender.)
  8. 8. 8PHYSIOLOGY OF GASTRIC ACID SECRETION:Gastric acid secretion is a complex, continuous process in which multiple centraland peripheral factors contribute to a common endpoint: the secretion of H+ byparietal cells. Neuronal (acetylcholine, ACh), paracrine (histamine), and endocrine(gastrin) factors all regulate acid secretion .Their specific receptors (M3, H2, andCCK2 receptors, respectively) are on the basolateral membrane of parietal cells inthe body and fundus of the stomach. The H2 receptor is a GPCR that activates theGs-adenylylcyclase-cyclic AMP-PKA pathway. ACh and gastrin signal throughGPCRs that couple to the Gq-PLC-IP3-Ca2+ pathway in parietal cells. In parietalcells, the cyclic AMP and the Ca2+-dependent pathways activate H+,K+-ATPase(the proton pump), which exchanges hydrogen and potassium ions across theparietal cell membrane. This pump generates the largest known ion gradient invertebrates, with an intracellular pH of about 7.3 and an intracanalicular Ph ofabout0.8.The most important structures for CNS stimulation of gastric acid secretion are thedorsal motor nucleus of the vagal nerve, the hypothalamus, and the solitary tractnucleus. Efferent fibers originating in the dorsal motor nuclei descend to thestomach via the vagus nerve and synapse with ganglion cells of the enteric nervoussystem. ACh release from postganglionic vagal fibers directly stimulates gastricacid secretion through muscarinic M3 receptors on the basolateral membrane ofparietal cells. The CNS predominantly modulates the activity of the entericnervous system via ACh, stimulating gastric acid secretion in response to the sight,smell, taste, or anticipation of food (the "cephalic" phase of acid secretion). AChalso indirectly affects parietal cells by increasing the release of histamine from theenterochromaffin-like (ECL) cells in the fundus of the stomach and of gastrin fromGcells in the gastric antrum. ECL cells, the source of gastric histamine secretion,usually are in close proximity to parietal cells. Histamine acts as a paracrinemediator, diffusing from its site of release to nearby parietal cells, where itactivates H2 receptors. The critical role of histamine in gastric acid secretion isdramatically demonstrated by the efficacy of H2-receptor antagonists in decreasinggastric acid secretionGastrin, which is produced by antral G cells, is the most potent inducer of acidsecretion. Multiple pathways stimulate gastrin release, including CNS activation,local distention, and chemical components of the gastric contents. Gastrin
  9. 9. 9stimulates acid secretion indirectly by inducing the release of histamine by ECLcells;a direct effect on parietal cells also plays a lesser role.Somatostatin (SST), which is produced by antral D cells, inhibits gastric acidsecretion. 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 theconsequent reduction of SSTs inhibitory effect may contribute to excess gastrinproduction.Gastric Defenses Against Acid. The extremely high concentration of H+ in thegastric lumen requires robust defense mechanisms to protect the esophagus and thestomach. The primary esophageal defense is the lower esophageal sphincter, whichprevents reflux of acidic gastric contents into the esophagus. The stomach protectsitself from acid damage by a number of mechanisms that require adequate mucosalblood flow, perhaps because of the high metabolic activity and oxygenrequirements of the gastric mucosa. One key defense is the secretion of a mucuslayer that protects gastric epithelial cells. Gastric mucus is soluble when secretedbut quickly forms an insoluble gel that coats the mucosal surface of the stomach,slows ion diffusion, and prevents mucosal damage by macromolecules such aspepsin. Mucus production is stimulated by prostaglandins E2 and I2, which alsodirectly inhibit gastric acid secretion by parietal cells. Thus, alcohol, aspirin, and
  10. 10. 10other drugs that inhibit prostaglandin formation decrease mucus secretion andpredispose to the development of acid-peptic disease. A second important part ofthe normal mucosal defense is the secretion of bicarbonate ions by superficialgastric epithelial cells. Bicarbonate neutralizes the acid in the region of themucosal 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.
  11. 11. 11A history of heartburn, gastroesophageal reflux disease (GERD) and use of certainforms of medication can raise the suspicion for peptic ulcer. Medicines associatedwith peptic ulcer include NSAID (non-steroid anti-inflammatory drugs) that inhibitcyclooxygenase, and most glucocorticoids (e.g. dexamethasone and prednisolone).In patients over 45 with more than two weeks of the above symptoms, the odds forpeptic ulceration are high enough to warrant rapid investigation by EGD (seebelow).The timing of the symptoms in relation to the meal may differentiate betweengastric and duodenal ulcers: A gastric ulcer would give epigastric pain during themeal, as gastric acid is secreted, or after the meal, as the alkaline duodenal contentsreflux into the stomach. Symptoms of duodenal ulcers would manifest mostlybefore the meal—when acid (production stimulated by hunger) is passed into theduodenum. 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 thepatients age. Furthermore, typical ulcers tend to heal and recur and as a result thepain may occur for few days and weeks and then wane or disappear. Usually,
  12. 12. 12children and the elderly do not develop any symptoms unless complications havearisen.Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3hours commonly accompanies ulcers. This pain can be misinterpreted as hunger,indigestion or heartburn. Pain is usually caused by the ulcer but it may beaggravated 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 thesternum, it may last from few minutes to several hours and it may be worse whenthe stomach is empty. Also, sometimes the pain may flare at night and it cancommonly be temporarily relived by eating foods that buffer stomach acid or bytaking anti-acid medication. However, peptic ulcer disease symptoms may bedifferent for every sufferer.It is also important to remember that the symptoms listed below can occur as aresult of other conditions, not just duodenal or gastric ulcers. These include gastroesophageal reflux disease (GERD), chronic dyspepsia without the presence ofulcers (often called non-ulcer or functional dyspepsia), gallbladder disease, liverdisease and other disorders. Once again, if you are concerned about yoursymptoms, it is important that you see your doctor about your stomach problems.common Symptoms of a Peptic UlcerThe most common symptom of a peptic ulcer is a gnawing or burning pain in theabdomen between the breastbone and navel. Duodenal ulcers typically causesymptoms 2 to 5 hours after meals, when the stomach is empty, and can be relievedby eating. Gastric ulcers, on the other hand, are classically made worse by eating.You may experience pain soon after meals, and food wont improve symptoms. Foreach, 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 seriousbleeding.Abdominal pain is a common symptom but it doesnt always occur. The pain candiffer a lot from person to person. • Feeling of fullness -- unable to drink as much fluid
  13. 13. 13 • 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 nightOther 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 lossAnyone 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 asbleeding in the digestive system or a hole in the wall of the stomach or duodenum,which can make someone very sickComplications • 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.
  14. 14. 14 • 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.• You have sudden, severe pain.• You keep losing weight.• Your pain doesnt go away when you take your medicine.• Your pain reaches to your back
  15. 15. 15CAUSES:For almost 100 years, doctors believed that stress, spicy foods, and alcohol causedmost ulcers. Now we know that most peptic ulcers are caused by a particularbacterial infection in the stomach and upper intestine, by certain medications, or bysmoking.In 1982, two doctors — Barry Marshall and Robin Warren — discovered a certainkind of bacteria that can live and grow in the stomach. Both doctors went on to winthe Nobel Prize for their discovery. The medical name for these bacteria isHelicobacter pylori (or H. pylori, for short). Today doctors know that most pepticulcers are caused by an infection from H. pylori.Experts believe that 90% of all people with ulcers are infected with H. pylori. Butstrangely enough, most people infected with H. pylori dont develop an ulcer.Doctors arent completely sure why, but think it may partly depend upon theindividual person — for example, those who develop ulcers may already have aproblem with the lining of their stomachs.Its also thought that some people may naturally secrete more stomach acid thanothers — and it doesnt matter what stresses theyre exposed to or what foods theyeat. Peptic ulcers may have something to do with the combination of H. pyloriinfection and the level of acid in the stomach
  16. 16. 16As many as half of the worlds population is infected with H. pylori. Those livingin developing countries or crowded, unsanitary conditions are most likely tocontract the bacterium, which is passed from person to person. H. pylori onlygrows in the stomach, and is usually contracted during childhood.Interestingly, many people have this organism in their stomach, but dont get anulcer or gastritis. Coffee drinking, smoking, and drinking alcohol increase yourrisk for an ulcer from H. PyloriA major causative factor (60% of gastric and up to 90% of duodenal ulcers) ischronic inflammation due to Helicobacter pylori that colonizes the antral mucosa.The immune system is unable to clear the infection, despite the appearance ofantibodies. Thus, the bacterium can cause a chronic active gastritis (type Bgastritis), resulting in a defect in the regulation of gastrin production by that part ofthe stomach, and gastrin secretion can either be decreased (most cases) resulting inhypo- or achlorhydria or increased. Gastrin stimulates the production of gastricacid 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 ulcerformation.Another major cause is the use of NSAIDs (see above). The gastric mucosaprotects itself from gastric acid with a layer of mucus, the secretion of which isstimulated by certain prostaglandins. NSAIDs block the function ofcyclooxygenase 1 (cox-1), which is essential for the production of these
  17. 17. 17prostaglandins. COX-2 selective anti-inflammatories (such as celecoxib or thesince withdrawn rofecoxib) preferentially inhibit cox-2, which is less essential inthe 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 dueto increased medical treatment, a greater proportion of ulcers will be due toincreasing NSAID use among individuals with pain syndromes as well as thegrowth of aging populations that develop arthritis.The incidence of duodenal ulcers has dropped significantly during the last 30years, while the incidence of gastric ulcers has shown a small increase, mainlycaused by the widespread use of NSAIDs. The drop in incidence is considered tobe a cohort-phenomenon independent of the progress in treatment of the disease.The cohort-phenomenon is probably explained by improved standards of livingwhich has lowered the incidence of H. pylori infections.Although some studies have found correlations between smoking and ulcerformation, others have been more specific in exploring the risks involved and havefound that smoking by itself may not be much of a risk factor unless associatedwith H. pylori infection.Some suggested risk factors such as diet, spiceconsumption and blood type, were hypothesized as ulcerogens (helping causeulcers) until late in the 20th century, but have been shown to be of relatively minorimportance in the development of peptic ulcers. Similarly, while studies havefound that alcohol consumption increases risk when associated with H. pyloriinfection, it does not seem to independently increase risk, and even when coupledwith H. pylori infection, the increase is modest in comparison to the primary riskfactor.Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors, alsocause multiple and difficult to heal ulcers.Stress
  18. 18. 18Researchers also continue to look at stress as a possible cause, or at leastcomplication, in the development of ulcers. There is debate as to whetherpsychological stress can influence the development of peptic ulcers. Burns andhead trauma, however, can lead to physiologic stress ulcers, which are reported inmany patients who are on mechanical ventilation.An expert panel convened by the Academy of Behavioral Medicine Researchconcluded that ulcers are not purely an infectious disease and that psychologicalfactors do play a significant role. Researchers are examining how stress mightpromote H. pylori infection. For example, Helicobacter pylori thrives in an acidicenvironment, and stress has been demonstrated to cause the production of excessstomach acid. This was supported by a study on mice showing that both long-termwater-immersion-restraint stress and H. pylori infection were independentlyassociated with the development of peptic ulcers.A study of peptic ulcer patients in a Thai hospital showed that chronic stress wasstrongly associated with an increased risk of peptic ulcer, and a combination ofchronic 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.Risks of Developing a Stomach Ulcer
  19. 19. 19 • 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 treatmentsDiagnosis: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 thesescreening tests.The most accurate way to diagnose H. pylori is through upper endoscopy of theesophagus, stomach, and duodenum. Because this procedure is invasive, it isgenerally only done on people suspected to have an ulcer, or who are at high riskfor ulcers or other complications from H. pylori, such as stomach cancer.Risk factors include being over 45 or having symptoms such as: • Anemia • Difficulty swallowing • Gastrointestinal bleeding • Unexplained weight loss
  20. 20. 20The diagnosis is mainly established based on the characteristic symptoms. Thestomach pain is usually the first to signal a peptic ulcer. In some cases, doctorsmay treat ulcers without diagnosing them with specific tests and observe if thesymptoms resolve, meaning their primary diagnosis was accurate.Confirming the diagnosis is made with the help of tests such as endoscopies orbarium contrast x-rays. The tests are typically ordered if the symptoms do notresolve after a few weeks of treatment, or when they first appear in a person who isover age 45 or who has other symptoms such as weight loss, because stomachcancer can cause similar symptoms. Also, when severe ulcers resist treatment,particularly if a person has several ulcers or the ulcers are in unusual places, adoctor may suspect an underlying condition that causes the stomach tooverproduce acid.An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as agastroscopy, is carried out on patients in whom a peptic ulcer is suspected. Bydirect 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 accuratepeptic ulcer diagnosis on their own is their inability to differentiate between pastexposure to the bacteria and current infection. Additionally, a false-negative ispossible with a blood test if the patient has recently been taking certain drugs, suchas antibiotics or proton pump inhibitors.
  21. 21. 21Diagnosis 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.
  22. 22. 22The 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 thisexam the patient will be asked to drink a tasteless liquid which contains the carbonas part of the substance that the bacteria breaks down. After an hour, the patientwill 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 testprovides the advantage of being able to monitor the response to treatment used tokill 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 nevercontains air). This leads to "free gas" within the peritoneal cavity. If the patientstands erect, as when having a chest X-ray, the gas will float to a positionunderneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on anerect chest X-ray or supine lateral abdominal X-ray, is an omen of perforatedpeptic ulcer disease.Macroscopic appearance:Gastric ulcers are most often localized on the lesser curvature of the stomach. Theulcer is a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smoothbase and perpendicular borders. These borders are not elevated or irregular in theacute form of peptic ulcer, regular but with elevated borders and inflammatorysurrounding in the chronic form. In the ulcerative form of gastric cancer theborders are irregular. Surrounding mucosa may present radial folds, as aconsequence of the parietal scarring.
  23. 23. 23Microscopic appearanceA gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosaeand muscularis propria, produced by acid-pepsin aggression. Ulcer margins areperpendicular and present chronic gastritis. During the active phase, the base of theulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissueand fibrous tissue. The fibrous base of the ulcer may contain vessels withthickened wall or with thrombosis.[19]Differential diagnosis of epigastric pain • Peptic ulcer • Gastritis • Stomach cancer • Gastroesophageal reflux disease • Pancreatitis • Hepatic congestion • Cholecystitis • Biliary colic • Inferior myocardial infarction • Referred pain (pleurisy, pericarditis) • Superior mesenteric artery syndrome
  24. 24. 24ANTIULCER DRUGS:Antiulcer drugs are medicines used to treat ulcers in the stomach and the upper partof 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 theduodenum (the upper part of the intestine). Those that form in the stomach arecalled gastric ulcers; in the duodenum, they are called duodenal ulcers. Both typesare referred to as peptic ulcers. For a long time, physicians thought that stress andcertain foods caused ulcers. Now they know that most ulcers are caused either byinfection with a bacterium called Helicobacter pylori or by long-term use of aspirinor other nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. Ineither case, something damages the barrier of mucus that normally protects thestomach and duodenum from the powerful acids and enzymes that the bodyproduces to digest food. When that happens, the acids and enzymes begin to eataway at the unprotected tissue, causing ulcers.Ulcers do not always cause symptoms. When they do, they usually cause agnawing or burning pain -- something like hunger pangs -- between the breastboneand the navel. The pain often occurs early in the morning or between meals andmay 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, theblood may show up in the form of black, tarry stools.In addition to antibiotics to clear up the Helicobacter pylori infection, physiciansuse several types of antiulcer drugs that reduce the amount of acid the stomachproduces or that protect the lining of the stomach and duodenum.Getting the proper treatment for ulcers is important, because ulcers can lead toserious complications, such as bleeding, swelling, and scarring. If the swelling andscarring are severe, the opening between the stomach and intestine may becomeblocked. Untreated ulcers may also eat through the wall of the stomach orduodenum. When that happens, bacteria and partially digested food may leak intothe body cavity and cause a life-threatening condition called peritonitis.The three basic types of antiulcer drugs are H2-blockers, acid pump inhibitors, andmucosal protective medications. H2-blockers block the production of histamine, asubstance that stimulates acid secretion. By blocking histamine, these drugs reducethe amount of acid the stomach produces. Examples of H2-blockers are cimetidine
  25. 25. 25(Tagamet), famotidine (Pepcid), nizatidine (Axid) and ranitidine (Zantac). Thesedrugs usually provide relief within a few days to a few weeks, depending on theseverity of the ulcer. H2-blockers usually are given for 6-8 weeks to encouragehealing. If the ulcers were caused by Helicobacter pylori, and the infection is nottreated, the ulcers will usually recur and must be treated again. However, ulcersusually do not come back when the underlying infection is treated. Ulcers causedby nonsteroidal anti-inflammatory drugs do not need treatment with antibiotics.Acid pump inhibitors completely block the production of stomach acid by stoppingthe final step in acid secretion. Omeprazole (Prilosec) is an acid pump inhibitor.Mucosal protective medications create a protective barrier that allows the ulcer toheal 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 physicianwho prescribed the drug or the pharmacist who filled the prescription for thecorrect dosage.Always take antiulcer drugs exactly as directed. Never take larger or more frequentdoses, and do not take the drug for longer than directed.Although most of the drugs discussed here are available in both prescription andnonprescription (over-the-counter) forms, the nonprescription forms come in lowerdoses and are not intended for the treatment of ulcers. Anyone who has ulcersshould be under a physicians care and should use the drugs and doses thephysician prescribes.Antiulcer drugs may mask the symptoms of stomach cancer. Anyone taking thesedrugs should make sure that his or her physician has ruled out the possibility ofcancer.Time may be needed for antiulcer medicines to relieve the pain. Be patient andkeep taking the medicine as directed, even if it does not seem to be working atfirst. Antacids may be used to relieve the pain during this time, unless thephysician 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 antiulcerdrug.Do not stop taking antiulcer drugs just because symptoms improve. Take themedicine for as long as the physician says to take it.
  26. 26. 26Smoking cigarettes may slow the healing of ulcers and make them more likely todevelop again after treatment. Ideally, avoid smoking completely while takingantiulcer drugs or at least, avoid smoking after taking the last dose of the day willencourage healing of the ulcer.Antiulcer drugs may affect the results of certain medical tests. Anyone who istaking antiulcer drugs should let the physician know before having skin tests forallergies 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 temporarilyconfused while taking the antiulcer drugs called H2-blockers. These includecimetidine (Tagamet), famotidine (Pepcid), nizatidine (Axid), and ranitidine(Zantac). If this happens, notify the physician who prescribed the medicine. Thesedrugs also increase the effects of alcohol, so anyone taking them should not drinkalcoholic beverages without first checking with a physician or pharmacist. Largeamounts 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 severestomach inflammation.People with certain medical conditions or who are taking certain other medicinescan have problems if they take antiulcer drugs. Before taking these drugs, be sureto let the physician know about any of these conditions: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 takingantiulcer drugs. The physician should also be told about any allergies to foods,dyes, preservatives, or other substances.The effects of taking antiulcer drugs duringpregnancy have not been fully studied. Women who are pregnant or plan tobecome pregnant should check with their physicians about whether to use antiulcerdrugs.Antiulcer drugs can pass into breast milk and may affect nursing babies. Womenwho are breastfeeding and need to take antiulcer drugs should check with theirphysicians. Not breastfeeding until treatment with the drugs is finished may benecessary.
  27. 27. 27Before using antiulcer drugs, people with any of these medical problems shouldmake 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 workor 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 thenose. These problems usually go away as the body adjusts to the drug and do notrequire medical treatment. Less common side effects, such as blurred or dimmedvision, constipation, itching, rash, sleeplessness, abnormal dreams, breast swellingor tenderness, and backache also may occur and do not need medical attentionunless 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 followingside effects occur, check with the physician who prescribed the medicine as soonas possible: • Confusion • Fast, slow, pounding, or irregular heartbeat • 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 takingantiulcer 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 maybe greater. Anyone who takes antiulcer drugs should let the physician know all
  28. 28. 28other medicines he or she is taking. Among the drugs that may interact with certainantiulcer drugs are:Aspirin Alcohol Antacids such as Mylanta and Maalox Blood-thinning drugs suchas 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 asamiodarone (Cordarone), tocainide (Tonocard), quinidine preparations such asQuinidex, and procainamide (Procan) Nicotine (in cigarettes or in smokingcessation drugs, such as Nicoderm and Nicorette).Anti Ulcer Drugs are medicines used to treat ulcers in the stomach and the upperpartofthesmallintestine.Purpose:The Anti Ulcer Drugs are used as part of the treatment for ulcers. Ulcers are soresor raw areas that form in the lining of the stomach or the duodenum (the upper partof the intestine). Those that form in the stomach are called Gastric Ulcers; in theduodenum, they are called Duodenal Ulcers. Both types are referred to as PepticUlcers. For a long time, physicians thought that stress and certain foods causedulcers.Now they know that most ulcers are caused either by infection with a bacteriumcalled Helicobacter Pylori or by long-term use of aspirin or other Non-SteroidalAnti-Inflammatory Drugs (NSAIDs), such as Ibuprofen. In either case, somethingdamages the barrier of mucus that normally protects the stomach and duodenumfrom the powerful acids and enzymes that the body produces to digest food. Whenthat happens, the acids and enzymes begin to eat away at the unprotected tissueulcers.1) H2 RECEPTOR ANTAGONISTNIZATIDINE
  29. 29. 29 NizatidineFAMOTIDINE FamotidineCIMETIDINE
  30. 30. 30 CimetidineRANITIDINE Ranitidine2) PROTON INHIBITORS
  31. 31. 31OMEPRAZOLE Omeprazole3) PROTETIVE AGENTSSUCRALFATE SucralfateMISOPROSTOL
  32. 32. 32 Misoprostol4) ANTIBIOTICSAMOXICILLIN AmoxicillinCOMMON SIDE EFFECTS.
  33. 33. 33Antiulcer DrugsBrand Name Possible Common Side Effects Include:(Generic Name)Axid (nitzatidine) Diarrhea, headache, nausea and vomiting, sore throatCarafate (sucralfate) Constipation, insomnia, hives, upset stomach, vomitingCytotec (misoprostol) Cramps, diarrhea, nausea, gas, headache, menstrual disorders (including heavy bleeding and severe cramping)Pepcid (famotidine) Constipation or diarrhea, dizziness, fatigue, feverPrilosec (omeprazole) Nausea and vomiting, headache, diarrhea, abdominal painTagamet (cimetidine) Headache, breast development in men, depres- sion and disorientationZantac(ranitidine Headache, constipation or diarrhea, joint painhydrochloride)DescriptionThe proton pump inhibitors block the secretion of gastric acid by the gastricparietal cells. The extent of inhibition of acid secretion is dose related. In somecases, gastric acid secretion is completely blocked for over 24 hours on a singledose. In addition to their role in treatment of gastric ulcers, the proton pumpinhibitors 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 parietalcells, inhibiting the secretion of gastric acid. These drugs are less effective than theproton 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 bythe intravenous route. The H-2 receptor blockers may also be used to treatheartburn and hypersecretory syndromes. When given before surgery, the H-2receptor blockers are useful in prevention of aspiration pneumonia.
  34. 34. 34Sucralfate (Carafate), a substituted sugar molecule with no nutritional value, doesnot inhibit gastric acid, but rather, reacts with existing stomach acid to form a thickcoating that covers the surface of an ulcer, protecting the open area from furtherdamage. 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 forprevention of stress ulcers, the type seen in patients exposed to physical stresssuch as burns and surgery. It has no systemic effects.Recommended dosageThe doses of the proton pump inhibitors and H-2 receptor blockers vary dependingon the drug and condition being treated. Consult individual references.The dose of sucralfate for acute ulcer therapy is 1 gram four times a day. After theulcer has healed, maintenance treatment may continue at 1 gram two times daily.PrecautionsThe proton pump inhibitors are generally well tolerated, and the most commonadverse effects are diarrhea, itching, skin rash, dizziness and headache. Muscleaches and a higher than normal rate of respiratory infections are among the otheradverse reactions reported. Omeprazole has an increased rate of fetal deaths inanimal studies. It is not known if these drugs are excreted in human milk, butbecause of reported adverse effects to infants in animal studies, it is recommendedthat proton pump inhibitors not be used by nursing mothers.The H-2 receptor blockers vary widely in their adverse effects. Although they aregenerally well tolerated, cimetidine may cause confusion in elderly patients, andhas an antiandrogenic effect that may cause sexual dysfunction in males.Famotidine has been reported to cause headache in 4.7% of patients. It isadvisable that mothers not take H-2 receptor blockers while nursing.Sucralfate is well tolerated. It is poorly absorbed, and its most common side effectis 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 allergicresponses. Because sucralfate releases small amounts of aluminum into the system,it should be used with caution in patients with renal insufficiency. There is noinformation available about sucralfates safety in breastfeeding.
  35. 35. 35InteractionsProton pump inhibitors may increase the pH of the stomach. This will inactivatesome antifungal drugs that require an acid medium for effectiveness, notableitraconazole and ketoconazole.H-2 receptor blocking agents have a large number of drug interactions. Consultindividualized references.KEY TERMSHypersecretory— Excessive production of a bodily secretion. The most commonhypersecretory syndrome of the stomach is Zollinger-Ellison Syndrome, asyndrome consisting of fulminating intractable peptic ulcers, gastric hypersecretionand hyperacidity, and the occurrence of gastrinomas of the pancreatic cells of theislets of Langerhans.Inflammation— Pain, redness, swelling, and heat that usually develop in responseto injury or illness.Mucous— Thick fluid produced by the moist membranes that line many bodycavities and structures.Nonsteroidal anti-inflammatory drug (NSAID)— A type of medicine used torelieve pain, swelling, and other symptoms of inflammation, such as ibuprofen orketoprofen.Sucralfate should not be used with aluminum containing antacids, because of therisk of increased aluminum absorption. Sucralfate may inhibit absorption andreduce blood levels of anticoagulants, digoxin, quinidine, ketoconazole, quinolonesand phenytoin.Treatment:Ulcers caused by H. pylori bacteria are generally treated with a combination ofmedications:
  36. 36. 36 • 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.Treatment involves a combination of medications to kill the H. pylori bacteria (ifpresent), and reduce acid levels in the stomach. This strategy allows your ulcer toheal 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 usesdifferent 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 bacteriaIf you have an ulcer without an H. pylori infection, or one that is caused by takingaspirin or NSAIDs, your doctor will likely prescribe a proton pump inhibitor for 8weeks.You may also be prescribed this type of medicine if you must continue takingaspirin 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. Surgerymay be needed if bleeding cannot be stopped with an EGD,
  37. 37. 37The best way to stop any further growth of your stomach ulcer is to follow ahealthy diet. It must contain non-acidic meals along with liquid meals. Sour agentslike lemon should be strictly avoided in the diet. [20] Younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists before EGD isundertaken. Bismuth compounds may actually reduce or even clear organisms,though the warning labels of some bismuth subsalicylate products indicate that theproduct should not be used by someone with an ulcer.Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may also beprescribed a prostaglandin analogue (Misoprostol) in order to help prevent pepticulcers, which may be a side-effect of the NSAIDs.When H. pylori infection is present, the most effective treatments are combinationsof 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 sometimeswith bismuth compound. An effective first-line therapy for uncomplicated caseswould be Amoxicillin + Metronidazole + Pantoprazole (a PPI). In the absence ofH. pylori, long-term higher dose PPIs are often used.Treatment of H. pylori usually leads to clearing of infection, relief of symptomsand eventual healing of ulcers. Recurrence of infection can occur and retreatmentmay be required, if necessary with other antibiotics. Since the widespread use ofPPIs in the 1990s, surgical procedures (like "highly selective vagotomy") foruncomplicated peptic ulcers became obsolete.Perforated peptic ulcer is a surgical emergency and requires surgical repair of theperforation. Most bleeding ulcers require endoscopy urgently to stop bleeding withcautery, injection, or clipping.Ranitidine provides relief of peptic ulcers, heartburn, indigestion and excessstomach acid and prevention of these symptoms associated with excessiveconsumption of food and drink. Ranitidine is available over the counter from apharmacy and works by decreasing the amount of acid the stomach producesallowing healing of ulcers. Zantac tablets contain Ranitidine 150mg as the activeingredient which can also be bought generically.
  38. 38. 38Balance diet:Stress free life style, healthy food habit, balanced diet rich in food and vegetablesare very important for keeping our body system healthy. Patient suffering frompeptic 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 ofwater, milk, etc., this too will keep the body temperature low and also controlsacidity. However, do not add sugar to the milk.Stressful life style is one of the root causes of several diseases. Patient sufferingfrom peptic ulcer should live a stress-free life, should go for morning and eveningwalk, and do mild exercises, and yoga and meditations. Never eat in hurry, takefood timely and full of nutrients, eat small meals 3-4 times a day, chew your foodproperly, all this will help in digestion of food, will prevent acidity and otherdiseases.Diets for Stomach UlcersThis diet is a guideline that may help to decrease gastric irritation and excessivegastric acid secretion. This diet may also help prevent uncomfortable side effectssuch 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.
  39. 39. 39 • 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 UlcerGiven below are the simplest and the most effective home remedies for thetreatment of peptic ulcers.Fenugreek (methi) seeds:Take 2-3 tablespoon of fenugreek (methi) seeds and boil it in a glass of water. Addlittle amount of soil to it. Allow the mixture to boil till it become half of its
  40. 40. 40constituent. Take this mixture 2-3 times a day, until the ulcer is not curedcompletely. One of the useful home remedies for peptic ulcers.Fruits:Among various other fruits, banana is considered as one of an effective fruit fortreating peptic ulcer. Banana helps in lowering the acidic substance inside thebody. 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 itinto water overnight. Drain the mixture and take this 2-3 times a day. This worksgreat 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 ofwater every day. Warm milk containing drops of castor oil is also very good fortreating peptic ulcer.Lemon:Lemon extract or juice is also very effective in treating peptic ulcer. Prepare freshlemon juice, add little amount of salt to it. This drink helps in digestion and hencehelps in treating peptic ulcers. This is one of the best home remedies for pepticulcers.Vegetables:Among vegetables cabbage is very useful for treating peptic ulcer. Cut cabbageinto small pieces, allow the vegetable to boil in water till the constituent becomehalf. Drain the mixture and take this 2-3 time a day. One can also add little amountof black pepper powder to it.Drumsticks:Drumstick leaves are also an effective home remedy for the treatment of pepticulcer. Take 15-20 leaves of drumstick and make its paste. Mix this paste in fresh
  41. 41. 41curd. Take this 2-3 times a day. This is one of the important home remedies forpeptic ulcers.Prevention:Doctors are not totally certain how H. pylori bacteria are transmitted from personto person. The bacteria have been found in saliva. They also may be spreadthrough food, water, or contact with vomit (puke) that has been infected with thebacteria.
  42. 42. 42The best advice in ulcer prevention is to always wash your hands after you use thebathroom and before you eat and to take good care of your body by exercisingregularly and not smoking or drinking.Avoid aspirin, ibuprofen, naproxen, and other NSAIDs. Try acetaminopheninstead. If you must take such medicines, talk to your doctor first. Your doctormay: • Test you for H. pylori first • Have you take proton pump inhibitors (PPIs) or an acid blocker • Have you take a drug called MisoprostolThe 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.
  43. 43. 43 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  Eating junk food shoud be avoided
  44. 44. 44  Long term use of asprin and NSAIDS should be prevented.Reference listFantry, G. T. (2005, May 6). Peptic Ulcer Disease. Retrieved September4th, 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
  45. 45. 45Microbe Wiki (2006, August 16). Heliobacter. Retrieved September 10th, 2006,from www.microbewiki.kenyon.edu/index.php/HelicobacterMoore, R. A. (1995). Helicobacter pylori and peptic ulcer: A systematic review ofeffectiveness and an overview of the economic benefits of implementing what isknown to be effective. Oxford: Cortecs Limited and Health Technology EvaluationAssociation.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-receptorantagonists.Gastroenterology, 1993, 105:963-968.PUBMEDChong, E., and Ensom, M.H. Pharmacogenetics of the proton pump inhibitors: asystematic review. Pharmacotherapy, 2003, 23:460-471. PUBMEDCook, D., Guyatt, G., Marshall, J., et al. Comparison of sucralfate and ranitidinefor the prevention of upper gastrointestinal bleeding in patients requiringmechanical ventilation. Canadian Critical Care Trials Group. N. Engl. J. Med.,1998, 338:791-797. PUBMEDDickson, E.J., and Stuart, R.C. Genetics of response to proton pump inhibitortherapy: clinical implications. Am. J. Pharmacogenomics, 2003, 3:303-315.PUBMEDFackler, W.K., Ours, T.M., Vaezi, M.F., and Richter, J.E. Long-term effect ofH2RA therapy on nocturnal gastric acid breakthrough.Gastroenterology, 2002, 122:625-632. PUBMEDFreston, J., Chiu, Y.L., Pan, W.J., Lukasik, N., and Taubel, J. Oral bioavailabilityof pantoprazole suspended in sodium bicarbonate solution. Am. J. Health Syst.Pharm., 2003, 60:1324-1329.Graham, D.Y. Therapy of Helicobacter pylori: current status and issues.
  46. 46. 46Gastroenterology, 2000, 118:S2-S8.Howden, C.W., and Hunt, R.H. Guidelines for the management of Helicobacterpylori infection. Ad Hoc Committee on the Practice Parameters of the AmericanCollege of Gastroenterology. Am. J. Gastroenterol., 1998, 93:2330-2338.PUBMEDKlinkenberg-Knol, E.C., Festen, H.P., Jansen, J.B., et al. Long-term treatment withomeprazole for refractory esophagitis: efficacy and safety. Ann. Intern.Med., 1994, 121:161-167. PUBMEDKuipers, E.J., and Meuwissen, S.G. The efficacy and safety of long-termomeprazole treatment for gastroesophageal reflux disease.Gastroenterology, 2000, 118:795-798. PUBMEDLanza, F.L. A guideline for the treatment and prevention of NSAID-inducedulcers. Members of the Ad Hoc Committee on Practice Parameters of theAmerican College of Gastroenterology. Am. J. Gastroenterol., 1998,93:2037-2046. PUBMEDRichter, J.E. Gastroesophageal reflux disease during pregnancy. Gastroenterol.Clin. North Am., 2003, 32:235-261. PUBMEDRostom, A., Dube, C., Wells, G., et al. Prevention of NSAID-inducedgastroduodenal 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: thepharmacological 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. PUBMEDWolfe, M.M., and Sachs, G. Acid suppression: optimizing therapy forgastroduodenal ulcer healing, gastroesophageal reflux disease, and stress-relatederosive syndrome. Gastroenterology, 2000, 118:S9-S31.

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