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INTRODUCTIONPhysiologically, a certain amount of acid is secreted by the gastric cells lining the stomach as a natural mechanism which serves to activate the digestive enzymes and help in the digestion and assimilation of important proteins so that they can be easily absorbed by the body.

Acid peptic disease is a collective term used to include many conditions such as gastro-esophageal reflux disease (GERD), gastritis, gastric ulcer, duodenal ulcer, esophageal ulcer, Zollinger Ellison Syndrome (ZES) and Meckels diverticular ulcer.

The commonest ulcers are the gastric and the duodenal ulcer.

Symptoms of peptic ulcers include abdominal pain, nausea, water brash, vomiting, loss of appetite and weight loss. Complications include bleeding, perforation, obstruction in the digestive tract and sometimes cancer.

Peptic ulcer is diagnosed using blood and stool tests, breath tests, and endoscopy and barium radiography. The patient is treated with drugs that reduce acidity and sometimes in addition with certain antibiotics to eliminate the H pylori causing the infection (described below). Surgery may be required in some cases.MEANINGAcid peptic disorders include a number of conditions whose pathophysiology is believed to be the result of damage from acid and pepsin activity in the gastric secretions. This talk focuses on gastro esophageal reflux disease (GERD) and peptic ulcer disease, the two most common and well defined disease statesPEPTIC ULCER DISEASEdefinition peptic ulcers(gastric and duodenal) are defects in the in the gastrointestinal mucosa that extend through the muscularis mucosa. CAUSES Acid peptic disease is a result of either a decreased gastric mucosal defense or an excessive acid production.

Causes of acid peptic disease include:

Helicobacter pylori: H.pylori is responsible for around 60%-90% of all gastric and duodenal ulcers.Gastrinstimulates the production ofgastric acidby parietal cells. InH. pyloricolonization responses to increased gastrin, the increase in acid can contribute to the erosion of themucosaand therefore ulcer formation. NSAIDs: Prostaglandins protect the mucus lining of the stomach. Non steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, diclofenac and naproxen prevent the production of these prostaglandins by blocking cyclo-oxygenase enzyme leading to ulceration and bleeding.

Smoking, alcohol and tobacco: Cigarettes, alcohol and tobacco cause an instant and intense acid production which acts as though gasoline is poured over a raging fire!

Blood group O: People with blood group O are reported to have higher risks for the development of stomach ulcers as there is an increased formation of antibodies against the Helicobacter bacteria, which causes an inflammatory reaction and ulceration.

Heredity: Patients suffering from peptic ulcer diseases usually have a family history of the disease, particularly the development of duodenal ulcer which may occur below the age of 20.

Steroids/Other medicines: Drugs like corticosteroids, anticoagulants like warfarin (Coumadin), niacin, some chemotherapy drugs, and spironolactone can aggravate or cause ulcers.

Diet: Low fiber diet, caffeinated drinks and fatty foods are linked to peptic ulcer.

Other diseases: Chronic liver, lung and kidney diseases especially tumors of the acid producing cells all predispose to peptic ulcers. Zollinger-Ellison Syndrome (ZES) is a rare pre-cancerous condition which causes peptic ulcer disease. It is a syndrome disorder wherein tumors in the pancreas and duodenum also known as gastrinomas produce a large amount of gastrin which is a hormone that stimulates gastric acid secretion. Endocrine disorders such as hyperparathyroidism are also implicated in the development of pepticulcers.

Stress: Stress and neurological problems can also be associated with the Cushing ulcer and peptic ulcer.Risk FactorsAlthough some studies have found correlations between smoking and ulcer formation.Some suggested risk factors such asdiet, andspiceconsumption, Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, Similarly alcohol consumption increases risk when associated withH. pyloriinfection, Gastrinomas(Zollinger Ellison syndrome), rare gastrin-secreting tumors, also cause multiple and difficult-to-heal ulcers.

CLASSIFICATIONBy region/area Duodenum(called duodenal ulcer) Esophagus(called esophageal ulcer) Stomach(called gastric ulcer) Meckel's diverticulum(called Meckel's diverticulum ulcer; is very tender with palpation)Gastric Ulcers Duodenal Ulcers Most common in late middle age middle age Incidence increase with age 30-50yrs Male to female ratio-2:1 4:1 Use of NSAID Genetic Link-ist degree relative, H.Pyloric infectionEsophageal ulcers

When peptic ulcers occur, they can be found in either the lining of the stomach, the lining of the duodenum, or in both. Peptic ulcers that occur in the stomach are named gastric ulcers whereas ulcers found in the duodenum are referred to as duodenal ulcers. Peptic ulcers can be minor (they only go through the first or the second layers of the stomach), or can be considered a medical emergency (they go through every layer of the stomach or duodenum lining causing major internal bleeding). A peptic ulcer is a defect that occurs in the first part of the small intestine or in the lining of the stomach. Small ulcers may not be noticeable, whereas large ulcers are considered medical emergencies. Abdominal pain is a common symptom seen with multiple types of ulcers. Common causes of ulcers can be: bacterial infections in the stomach or duodenum, a weakening of the stomach lining caused by a continuous use of an anti inflammatory, or the common.PATHOPHYSIOLOGYPeptic ulcer disease encompasses gastric, duodenal, and esophageal ulcers, with common etiologies of Helicobacterpyloriinfection, NSAID use, and stress-related mucosal damage . Ulcers may occur with hypersecretion of hydrochloric acid and pepsin, causing an imbalance between gastric luminal factors and degradation in the defensive function of the gastric mucosal barrier. Mucosal defenses include: Mucus secretion of bicarbonate mucosal blood flow, and epithelial cell defense. When acid and pepsin invade a weakened area of the mucosal barrier, histamine is released. Histamine will stimulate parietal cells to secrete more acid. With the continuation of this vicious cycle, erosion occurs to form the ulcer.Although over 50% of the population has chronicH pyloriinfection, only 5% to 10% develop ulcers.Hpyloriis a pH-sensitive bacterium that can infiltrate the gastric mucosal layer to reside in a neutral-pH environment. Acutely, the infection or colonization may ironically produce a hypochlorhydric environment. It is thought that this protective mechanism for the organism occurs due to the increase of urease, which hydrolyzes urea and converts it to ammonia and carbon dioxide.H pyloricontributes to mucosal injury by multiple mechanisms Ulcers induced by nonselective NSAIDs can occur due to a topical irritation of the gastric epithelial cells and reduced protective prostaglandin synthesis.Due to their pharmacologic properties, many acidic NSAIDs cause alterations in the hydrophobic mucosal gel layer. The topical irritation may be the first insult to injury; however, inhibition of cyclooxygenase (COX) is the greatest concern. NSAIDs inhibit the rate-limiting enzyme in the conversion of arachidonic acid to prostaglandins. COX-2 exists throughout the body, producing prostaglandins associated with inflammation and pain, whereas COX-1 is located in the stomach, kidney, intestines, and platelets. Isoforms COX-1 and COX-2 are inhibited by nonselective NSAIDs. As a result of COX-1 inhibition, adverse effects such as ulcers or GI bleeds may occur.SIGNS AND SYMPTOMSSymptoms of a peptic ulcer can be abdominal pain, classicallyepigastricstrongly correlated to mealtimes. In case of duodenal ulcers the pain appears about three hours after taking a meal; Dull, gnawing pain and a burning sensation in the mid epigastrium or in the back are characteristic. Pain is relieved by eating or taking alkali; once the stomach has emptied or the alkali wears off, the pain returns. Sharply localized tenderness is elicited by gentle pressure onthe epigastrium or slightly right of the midline. Other symptoms include pyrosis (heartburn) and a burningsensation in the esophagus and stomach, which moves up tothe mouth, occasionally with sour eructation (burping). bloatingand abdominal fullness; waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus - although this is more associated withgastroesophageal reflux disease); 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 presence ofoxidizediron fromhemoglobin); rarely, an ulcer can lead to a gastric orduodenal perforation, which leads The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would giveepigastricpain during the meal, asgastric acidproduction is increased as food enters the stomach. Symptoms of duodenal ulcers would initially be relieved by a meal, as thepyloric sphinctercloses to concentrate the stomach contents, therefore acid is not reaching the duodenum. Duodenal ulcer pain would manifest mostly 23hours after the meal, when thestomach begins to release digested food and acid into theduodenum.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, children and theelderlydo not develop any symptoms unless complications have arisen.Burning or gnawing feeling in the stomach area lasting between 30minutes and 3hours commonly accompanies ulcers. This pain can be misinterpreted ashunger,indigestionorheartburn. Pain is usually caused by the ulcer but it may be aggravated by thestomach acidwhen 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 when the stomach is empty. Also, sometimes the pain may flare. DIAGNOSTIC MESURESThe diagnosis is mainly established based on the characteristic symptoms. History collection-Stomach pain is usually the first signal of a peptic ulcer. In some cases, doctors may treat ulcers without diagnosing them with specific tests and observe whether the symptoms resolve, thus indicating that their primary diagnosis was accurate.Confirmation of the diagnosis is made with the help of tests such as endoscopies or barium contrastx-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 asweight loss, becausestomach cancercan 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 overproduceacid.Anesophagogastroduodenoscopy(EGD), a form ofendoscopy, also known as agastroscopy, 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 thatblood testsare not reliable for 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 result is possible with a blood test if the patient has recently been taking certain drugs, such asantibioticsorproton pump inhibitors.The diagnosis ofHelicobacter pylorican 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 performH. pyloricultures; Direct detection ofureaseactivity in a biopsy specimen byrapid urease test; Measurement ofantibodylevels in blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy; Stoolantigentest; Histological examination and staining of an EGD biopsy.The breath test uses radioactivecarbon atomto 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 radioactivecarbon dioxide. This test provides the advantage of being able to monitor the response to treatment used to kill the bacteria.The possibility of other causes of ulcers, notablymalignancy(gastric cancer) needs to be kept in mind. This is especially true in ulcers of thegreater (large) curvatureof thestomach; most are also a consequence of chronicH. pyloriinfection.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.TREATMENTYounger patients with ulcer-like symptoms are often treated withantacidsorH2 antagonistsbefore EGD is undertaken.Patients who are takingnonsteroidal anti-inflammatories(NSAIDs) may also be prescribed aprostaglandinanalogue(Misoprostol) in order to help prevent peptic ulcers, which are aside-effectof the NSAIDs.WhenH. pyloriinfection is present, the most effective treatments are combinations of 2 antibiotics (e.g.Clarithromycin,Amoxicillin,Tetracycline,Metronidazole) and 1proton 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 ofH. pylori, long-term higher dose PPIs are often used.Treatment ofH. pyloriusually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Ranitidineandfamotidine, which are both H2 antagonists, provide relief of peptic ulcers, heartburn, indigestion and excess stomach acid and prevention of these symptoms associated with excessive consumption of food and drink. Ranitidine and famotidine are available over the counter at pharmacies, both as brand-name drugs and as generics, and work by decreasing the amount of acid the stomach produces allowing healing of ulcers.Sucralfate(Carafate) has also been a successful treatment of peptic ulcers.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, orclipping.SURGICAL MANAGEMENTWith the advent of H2receptor antagonists, surgical intervention is less common.If recommended, surgery is usually for intractable ulcers(particularly with ZollingerEllison syndrome), lifethreatening hemorrhage, perforation, or obstruction. Surgicalprocedures include vagotomy, vagotomy with pyloroplasty,or Billroth I or II. Billroth I, more formallyBillroth's operation I, is anoperationin which thepylorusis removed and the proximalstomachisanastomoseddirectly to theduodenum. Billroth II, more formallyBillroth's operation II, is anoperationin which thegreater curvatureof the stomach is connected to the first part of the jejunumin a side-to-side manner. This often follows resection of the lower part of the stomach(antrum). The antrectomy (resection of thestomach antrum) is not part of the originally described procedure. The surgical procedure is calledgastrojejunostomy.The Billroth II is often indicated in refractorypeptic ulcer diseaseandgastric adenocarcinoma. It was first described byTheodor Billroth.Complications Gastrointestinal bleedingis the most common complication. Sudden large bleeding can be life-threatening, though this is more common in the elderly population.It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery. Perforation(a hole in thewall of the gastrointestinal tract) often leads to catastrophic consequences if left untreated. 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 acuteperitonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain; an example isValentino's syndrome, named after the silent-film actor who experienced this pain before his death. Posterior wall perforation leads to bleeding due to involvement of gastroduodenal artery that lies posterior to the 1st part of duodenum. Perforationandpenetrationare when the ulcer continues into adjacent organs such as the liver andpancreas. Gastric outlet obstructionis the narrowing of pyloric canal by scarring and swelling of gastric antrum and duodenum due to peptic ulcers. Patient often presents with severe vomiting without bile. Cancer is included in the differential diagnosis (elucidated bybiopsy),Helicobacter pylorias the etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.NURSING ASSESSMENT Assess pain and methods used to relieve it; take a thorough history, including a 72hour food intake history. If patient has vomited, determine whether emesis isbright red or coffee ground in appearance. This helpsidentify source of the blood. Ask patient about usual food habits, alcohol, smoking, medication use (NSAIDs), and level of tension or nervousness. Ask how patient expresses anger (especially at work andwith family), and determine whether patient is experiencing occupational stress or family problems. Obtain a family history of ulcer disease. Assess vital signs for indicators of anemia (tachycardia,hypotension). Assess for blood in the stools with an occult blood test. Palpate abdomen for localized tenderness.NURSING DIAGNOSIS Acute Pain related to the effect of gastric acid secretionon damaged tissue Anxiety related to coping with an acute disease Imbalanced Nutrition related to changes in diet Decient Knowledge about preventing symptoms and managing the conditionPotential Complications Hemorrhage: upper GI Perforation Penetration Pyloric obstruction (gastric outlet obstruction)Planning and Goals The major goals of the patient may include relief of pain,reduced anxiety, maintenance of nutritional requirements,knowledge about the management and prevention of ulcerrecurrence, and absence of complications.NURSING INTERVENTIONSRelieving Pain and Improving Nutrition Administer prescribed medications. Avoid aspirin, which is an anticoagulant, and foods andbeverages that contain acidenhancing caffeine (colas, tea,coffee, chocolate), along with decaffeinated coffee. Encourage patient to eat regularly spaced meals in arelaxed atmosphere; obtain regular weights and encouragedietary modications. Encourage relaxation techniques.Reducing Anxiety Assess what patient wants to know about the disease, andevaluate level of anxiety; encourage patient to expressfears openly and without criticism. Explain diagnostic tests and administering medications onschedule. Interact in a relaxing manner, help in identifying stressors,and explain effective coping techniques and relaxationmethods. Encourage family to participate in care, and giveemotional support.MONITORING AND MANAGING COMPLICATIONSIf hemorrhage is a concern Assess for faintness or dizziness and nausea, before or with bleeding; test stool for occult or gross blood;monitor vital signs frequently (tachycardia, hypotension,and tachypnea). Insert an indwelling urinary catheter and monitor intakeand output; insert and maintain an IV line for infusinguid and blood. Monitor laboratory values (hemoglobin and hematocrit). Insert and maintain a nasogastric tube and monitordrainage; provide lavage as ordered. Monitor oxygen saturation and administering oxygentherapy. Place the patient in the recumbent position with the legselevated to prevent hypotension, or place the patient onthe left side to prevent aspiration from vomiting. Treat hypovolemic shock as indicated.If perforation and penetration are concerns Note and report symptoms of penetration (back and epigastric pain not relieved by medications that wereeffective in the past). Note and report symptoms of perforation (sudden abdominal pain, referred pain to shoulders, vomiting andcollapse, extremely tender and rigid abdomen,hypotension and tachycardia, or other signs of shock).Home and CommunityBased CareTEACHING PATIENTS SELFCARE Assist the patient in understanding the condition and factors that help or aggravate it. Teach patient about prescribed medications, including name,dosage, frequency, and possible side effects. Also identifymedications such as aspirin that patient should avoid. Instruct patient about particular foods that will upset thegastric mucosa, such as coffee, tea, colas, and alcohol,which have acidproducing potential. Encourage patient to eat regular meals in a relaxed settingand to avoid overeating. Explain that smoking may interfere with ulcer healing;refer patient to programs to assist with smokingcessation. Alert patient to signs and symptoms of complications tobe reported. These complications include hemorrhage(cool skin, confusion, increased heart rate, labored breathing, and blood in the stool), penetration and perforation(severe abdominal pain, rigid and tender abdomen, vomiting, elevated temperature, and increased heart rate), andpyloric obstruction (nausea, vomiting, distended abdomen,and abdominal pain). To identify obstruction, insert andmonitor nasogastric tube; more than 400 mL residual suggests obstruction.EVALUATIONExpected Patient Outcomes Remains free of pain between meals Experiences less anxiety Complies with therapeutic regimen Maintains weight