PEPTIC ULCER DISEASE - pharmacytechtopics.com · 10/31/2012 · Describe the pathophysiology of peptic ulcer disease. 2. List the risk factors for developing peptic ulcer disease

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Home-Study Continuing Pharmacy Education MODULESfor Nationally CertifiedPharmacy Technicians

OCTOBER 2010 VOLUME 15 NUMBER 4

PEPTIC ULCER DISEASE

echopicsTM

BY ICHP

PHARMACY

Pharmacy Tech TopicsTM is provided as a free serviceto all Pharmacy Technician Members of the AmericanSociety of Health-System Pharmacists.

Peptic Ulcer Disease

3

This module is accredited for 2.5 contact hours of continuing pharmacy education and isrecognized by the Pharmacy Technician Certification Board (PTCB).

LEARNING OBJECTIVES

Upon completion of this module, the subscriber will be able to:

1. Describe the pathophysiology of peptic ulcer disease. 2. List the risk factors for developing peptic ulcer disease and the symptoms of peptic ulcer disease. 3. Identify the medications used for the initial therapy and maintenance therapy of peptic ulcer disease. 4. Recognize the appropriate dosage of medications used for peptic ulcer disease. 5. Explain the importance of patient adherence to the treatment plan for peptic ulcer disease.

Pharmacy Tech Topics™VOLUME 15 ISSUE 4

OCTOBER 2010

PEPTIC ULCER DISEASEEDITOR: Patricia M. Wegner, PharmD, FASHP

DESIGN EDITOR: Barbara J. Yahn

Pharmacy Tech Topics™ (USPS No. 014-766) is published quarterly for $50 per year by the Illinois Council of Health-System Pharmacists, 4055 N. Perryville Road, Loves Park, IL 61111-8653. Phone (815) 227-9292. PeriodicalsPostage Paid at Rockford, IL and additional mailing offices.

POSTMASTER: Send address changes to: Pharmacy Tech Topics,™ c/o ICHP, 4055 N. Perryville Road, Loves Park, IL 61111-8653

Copyright OCTOBER 2010

All contents ! 2010 Illinois Council of Health-System Pharmacists unless otherwise noted. All rights reserved.Pharmacy Tech Topics™ is a trademark of the Illinois Council of Health-System Pharmacists.

Accreditation: Pharmacy Tech TopicsTM Modules are accredited for Continuing Pharmacy Education (CPE) credits by theIllinois Council of Health-System Pharmacists. The Illinois Council of Health-System Pharmacists is accredited by theAccreditation Council for Pharmacy Education as a provider of continuing pharmacy education. !2010 Illinois Council ofHealth-System Pharmacists. Pharmacy Tech TopicsTM is a trademark of the Illinois Council of Health-System Pharmacists.The intended audience is pharmacy technicians.

This module will provide 2.5 hours of continuing pharmacy education credit for certified pharmacy technicians.ACPE Universal Activity Number: 121-000-10-004-H01-T Type of Activity: KnowledgeValidation Dates: 10/01/10 to 10/31/12

NOTICE

Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge,changes in treatment and drug therapy are required. The author and the publisher of this work havechecked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the author nor the publisher nor anyother party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they are not responsible for anyerrors or omissions or for the results obtained from use of such information. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers areadvised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this module is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs.

Pharmacy Tech TopicsTM OCTOBER 2010 FACULTY DISCLOSURE

It is the policy of the Illinois Council of Health-System Pharmacists (ICHP) to insure balance and objectivity inall its individually or jointly presented continuing pharmacy education programs. All faculty participating in anyICHP continuing pharmacy education programs are expected to disclose any real or apparent conflict(s) ofinterest that may have any bearing on the subject matter of the continuing pharmacy education program.Disclosure pertains to relationships with any pharmaceutical companies, biomedical device manufacturers, orother corporations whose products or services are related to the subject matter of the topic.

The intent of disclosure is not to prevent the use of faculty with a potential conflict of interest from authoring a publication but to let the readers know about the relationship prior to participation in the continuing pharmacy education activity. It is intended to identify financial interests and affiliations so that, with full disclosure of thefacts, the readers may form their own judgments about the content of the learning activity.

Dr. Sneha Srivastava’s submission has been peer reviewed with consideration and knowledge of these potential conflicts and it has been found to be balanced and objective. The author has no real or apparentconflict(s) of interest that may have any bearing on the subject matter of this continuing pharmacy educationprogram.

Pharmacy Tech TopicsTM RENEWAL information for 2011 found on page 25 of this module.

Renew Now for 2011!

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PHARMACY TECH TOPICSTM — OCTOBER 2010

Meet the AuthorSneha Srivastava, PharmD

Sneha Srivastava, PharmD is an Assistant Professor of PharmacyPractice at Chicago State University College of Pharmacy. Dr. Srivastava received her Doctor of Pharmacy degree in 2004 fromthe Ernest Mario School of Pharmacy at Rutgers University. She also completed a Pharmacy Practice Residency and then an AmbulatoryCare Specialty Residency at the University of Illinois at Chicago. She served on the faculty of the University of Connecticut School ofPharmacy in Storrs, CT from 2006-2008.

Dr. Srivastava’s clinical interests include diabetes, hypertension, hyperlipidemia, HIV/AIDS,and tobacco dependence, ambulatory and community care, as well as patient educationand outreach. Her research interests include medication adherence and health psychology in conjunction with the aforementioned disease states as well as the scholarship of teaching.


INTRODUCTIONPeptic ulcer disease (PUD) is defined as

erosions in the gastrointestinal tract secondaryto mucosal damage often caused by pepsin andgastric acid secretion.1 The erosions penetratethe muscularis mucosa and usually occur in thestomach, pylorus, duodenum, jejunum, ileum,and near Meckel’s diverticula; erosions and gastritis usually do not penetrate the mucosa asdeep. Helicobacter pylori (H. pylori) associated,nonsteroidal anti-inflammatory drug (NSAID)-induced and stress ulcers are the most common form of peptic ulcers. The stomach and duodenum are the most common places forNSAID-induced and H. pylori ulcers to occurwhile stress ulcers more often occur in the critically ill patient’s stomach.2 Peptic ulcer disease has a 60 to 100% rate of ulcers reoccurring within one year of initial ulcer.

Reprinted with permission from the National Digestive DiseasesInformation Clearinghouse.

http://digestive.niddk.nih.gov/ddiseases/pubs/pepticulcers_ez/index.htm

Figure 1. Diagram of the stomach

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EpidemiologyThere are many theories about the etiology

of peptic ulcers because of the shift in the patterns of gastritis. The first description of agastric ulcer was made in 1835 and in the beginning, gastric ulcers were found mostly inyoung females. In the 1900s, duodenal ulcersbecame more prevalent and the total number ofulcers diagnosed increased as well. Theoriesstate that environmental factors such as bettertransportation and refrigeration of food, leadingto the use of fewer preservatives, especially salt,caused the shift in patterns. Also, the moredeveloped countries have a lower incidence ofH. pylori because of better hygiene.3

The annual incidence of peptic ulcers is 0.1to 0.3%, increasing to 1% in patients with H. pylori. The lifetime prevalence is 5 to 10%(versus 10 to 20% in patients with H. pylori). Inwestern countries, the occurrence of ulcers issimilar in both sexes (although duodenal ulcerswere twice as common in men in the past); whilein Asian countries, duodenal ulcers are morecommon in males.3 Duodenal ulcers tend tooccur between 25 and 55 years of age; gastriculcers are more likely to occur between 40 and75 years of age. The estimated mortality (death) rate is 2.5 per 100,000 individuals.Epidemiologic studies have linked the prevalence of peptic ulcers to cigarette smoking,genetic factors, personality profiles, and H. pylori.3

Although there have been less physician visits, hospitalizations, operations, and deathsdue to peptic ulcer disease in general, hospitalizations and deaths of older adults haveincreased due to complications of ulcers. Thismay be linked to increased use of NSAIDs in theolder population and because gastric ulcers aremore common and associated with a highermortality (death) rate.2

Physiology of the GastrointestinalTract

Prior to discussing the pathologic process ofpeptic ulcer disease, it is necessary to review the

anatomy and physiology of the alimentary canal,also know as the gastrointestinal (GI) tract, inparticular the parts of the GI tract that may beaffected by the ulcers. The GI tract includes themouth, pharynx, esophagus, stomach, smallintestine, and large intestine. The process ofdigestion begins with mastication, where food ischewed and mixed with saliva followed by deglutition, the act of swallowing. The food passes through the pharynx and esophagusprior to reaching the stomach, where gastricdigestion transforms it to chyme, a liquid orsemiliquid consistency, by way of peristalsis ormuscular contractions. Chyme then travelsthrough the duodenum on its way to the small intestine. Simultaneously, the mucousmembrane of the stomach is secreting gastricjuice produced by both the sight of food and irritation on the mucous membrane due to thepresence of food in the stomach. Gastric juice, athin colorless liquid with a normal acidity level of0.02%, contains hydrochloric acid, pepsinogen,rennin, water, ammonium, calcium, potassium,and sodium chloride. Pepsin, an enzyme only present in acidic medium, is made by the conversion of pepsinogen in the presence ofhydrochloric acid.4

The secretion of gastric juice is stimulated byendogenous chemicals, such as acetylcholine,gastrin, and histamine. Acetylcholine, which isthought to be a neurotransmitter, is releasedupon vagal stimulation by acid secretion whenone sees, smells, tastes, chews, or thinks aboutfood. Gastrin is a hormone released by proteinsin food, vagal stimulation, calcium, magnesium,aluminum, and alkalinization of the antrum.Histamine, found in mastlike cells located inclose proximity to parietal cells of the stomach,causes acid secretion by acting on receptors on parietal cells much like acetylcholine andgastrin.4

As aforementioned, hydrochloric acid andpepsin play major roles in peptic ulcer disease.Physiologically, the body has a basal acid outputand a maximum acid output. The amount of acidsecreted while fasting is considered the basalacid output; the amount of acid secreted when

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injected with histamine is the maximum acid out-put which reflects the number of parietal cells.The number of parietal cells functioning underbasal conditions is shown by the ratio of basalacid output to maximum acid output. The basalcell output and ratio increase when there is an increase in the amount of acetylcholine, gastrin, and histamine near the parietal cells,causing basal acid hypersecretion. Cholinergic stimulation mediates not only the secretion ofpepsinogen into the gastric lumen but also itsconversion to pepsin under acidic conditions.

Endogenous prostaglandins utilize mucus,bicarbonate, mucosal blood, and cell renewal aspossible defense mechanisms against possibleaggressive factors that may cause damage tothe mucosa such as, acid, pepsin, bile, and pancreatic enzymes. The respective roles ofthese defense mechanisms are to form a protective coat over mucosal cells; allow for a pHgradient between the acidic lumen environmentand the mucosal surface; remove acid from themucosa; and maintain mucosal integrity.4

PathophysiologyThere is no single factor that explains why

ulcers occur.3 One factor is an abnormality in thesecretion of acid and pepsin. Acid secretion ishigher in about 30 to 40% of patients with duodenal ulcers, however, it is normal in mostpatients with gastric ulcers except those withZollinger-Ellison syndrome. Normal acid secretion rate does not preclude acid and pepsinas being factors in causing the ulcer.Additionally, bile and pancreatic juice reflux isthought to cause damage to the gastric mucosaby altering mucosal epithelial cells and disrupting the pH gradient formed, thus allowingthe mucosa to become permeable to acid andpepsin. Also, there may be a reduced amount ofmucus, mucosal blood flow, and bicarbonatesecretion in patients with ulcers. Although notclearly proven, emotional stress is thought toincrease gastric acidity while delayed gastricemptying is thought to cause gastritis by refluxing the duodenal contents back into the

stomach, both of which would damage gastricmucosa.4

The two most common causes of pepticulcers are Helicobacter pylori (H. pylori) infectionand the use of nonsteroidal anti-inflammatorydrugs (NSAIDs).1 Less common causes of ulcers include: cigarette smoking, infection, herpes simplex virus, cytomegalovirus, tubercu-losis, syphilis, medication induced (sirolimus,mycophenolate mofetil, potassium chloride,chemotherapy), hormonal or mediator-induced,gastrinoma, systemic mastocytosis, basophiliain myeloproliferative disease, astral G cell hyperfunction, post surgical, antral exclusion,post-gastric bypass, vascular insufficiency,crack/cocaine use, duodenal obstruction, radiation therapy, infiltrating disease, sarcoido-sis, and Crohn’s disease.3 In a study comparingsmokers to never smokers in Brazil, pepticulcers were found in 56.9% of smokers versus28.3% in never smokers, a statistically signifi-cant difference.5 Although the mechanism isunclear, other epidemiologic studies have alsofound positive correlations between smokersand peptic ulcer disease. This includes higherrates of PUD in those who smoke morecigarettes, higher rates of deaths due to PUD in smokers, and less healing as well as the reoccurrence of duodenal ulcers in smokers.4 Medications, other than NSAIDs,have conflicting data regarding their contribu-tion, or lack thereof, to PUD. In addition, there isno evidence that alcohol and caffeine causepeptic ulcer disease even though they doincrease acid production.4

Pathophysiology of H. pylori-induced PUD

H. pylori is present in almost half of theworld’s population.4 Protective roles of H. pylorihave been speculated including low incidencesof gastroesophageal reflux disease (GERD) andchildhood diarrhea. H. pylori may be spread dueto a contaminated water supply and many developing countries have developed a drugresistance to local strains of it.6 Although many

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people harbor H. pylori, approximately 20% willdevelop peptic ulcer disease and less than onepercent will develop gastric cancer. H. pylori isnot a typical bacterial pathogen, it is able to survive in the acidic environment of the stomachand it causes disease not only by releasing toxins but also by interaction with its host andenvironment. It is also the first bacterialpathogen known to cause cancer.6

The stomach may be colonized with H. pylorifor years, causing continuous inflammation. Thisbacterial colonization, usually inhibited by peristalsis and gastric acidity, is allowed for by constituents of H. pylori such as urease, flagellae, adhesins, vasculating cytotoxin, andCagA. Urease targets gastric acid by neutraliz-ing acidity while flagellae and adhesins targetgastric peristalsis because of their function ofmotility and adherence to gastric epithelium,respectively. Although in vitro (outside of thebody) studies show that H. pylori is susceptibleto the antibodies formed; H. pylori is able to existin vivo (inside of the body), suggesting that thegastric mucosa may provide a protective environment against the antibodies formed.4

There are several mechanisms of H. pyloriinduced inflammation that are postulated. Onemechanism is that inflammation occurs becauseof cytokine release secondary to direct contactof H. pylori with gastric epithelial cells. This canbe spread by the fecal-oral route, oral-oral route,or through iatrogenic ways, such as via an endoscopic tube if improperly cleaned.2

Pathophysiology of NSAIDInduced Ulcers

Mucosal injury to the upper gastrointestinaltract, leading to peptic ulcer disease and possibly upper gastrointestinal hemorrhage andperforation, may be caused by NSAID use. It isestimated that 25% of chronic NSAID users willdevelop PUD with bleeding or perforation inabout 2 to 4% of cases. The hospital admissionrate is about 100,000 cases per year and thereare about 7,000 to 10,000 deaths annually secondary to NSAID-related gastrointestinal

events.7 Meta-analysis studies (studies that statistically analyze several studies that are similar to look for stronger significance of theresults) have identified certain characteristicsthat place patients in the category of having ahigh risk of NSAID-related gastrointestinal complications. These risk factors include: previous gastrointestinal event, age, drug interactions, high-dose NSAID therapy, chronicdebilitating disorders (especially cardiovasculardisease), concurrent low-dose aspirin, genetics,and H. pylori infection.7

Each of the risk factors should be consideredin detail. There is a higher risk associated withcomplicated and/or more recent gastrointestinalevents. Generally, age above 75 years old isconsidered a higher risk. There are several medication interactions that increase the risk ofNSAID-induced events. This includes concurrentuse of multiple NSAIDs, low dose aspirin, selective serotonin reuptake inhibitors,alendronate, corticosteroids, and clopidogrel.Additionally, since H. pylori infection was shownto increase the risk of NSAID-related gastroin-testinal events, the guidelines also concludedthat testing for and possibly eradicating H. pylorimay be advantageous in patients that requirelong-term NSAID therapy.7

Aspirin and PUDA study looked at 156 adults with a history of

cardiovascular disease who had peptic ulcerbleeding and were treated with endoscopic therapy. These patients were then randomizedto either aspirin 80mg daily or placebo for 8weeks. The researchers found that about 10% ofthe patients assigned to aspirin had a recurrentulcer bleed within 30 days. Five percent of thepatients in the placebo group had a recurrentulcer bleed. Additionally, they found that 10 of 78patients in the placebo group died at 8 weeksversus 1 of 78 patients in the aspirin group. Thedeaths in the placebo group were due to acutecoronary syndrome, stroke, heart failure, perforated ulcer and pneumonia. The one deathin the aspirin group was due to heart failure.Since this was a small study, no absolute

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conclusions can be made. This study suggeststhat continued aspirin use after a peptic ulcerbleed increases chances of recurrent bleedingand that reduction in death with aspirin useneeds to be further studied.8

Clinical Presentation Symptoms usually occur in two thirds of

patients with ulcers. The most common symptoms include dyspepsia (heartburn), usually manifesting as nausea, vomiting,anorexia, fullness, and/or bloating.1 Dyspepsia isalso common in other gastrointestinal diseases,so it can not be used alone to diagnose PUD.4

Patients may also complain of recurrent post-prandial (after meal) epigastric pain. Typically,pain in the epigastrium is described as burningor gnawing comparable to hunger pangs. Theoccurrence of pain is usually episodic with eachepisode lasting minutes and occurring in clusterslasting from days to weeks or there may be longperiods of no pain. If the pain changes in character, it could be due to perforation or penetration.

The aforementioned symptoms require further evaluation to diagnose peptic ulcer disease. When a patient presents with certainalarm symptoms, they should be directed to theirhealth care provider immediately for evaluationas these symptoms may suggest complicationsof ulcers. Alarm symptoms include: anemia,hematemesis (throwing up blood), melena(blood in stool), or heme-positive stool, vomiting,anorexia or weight loss, persisting upper abdominal pain radiating to the back, andsevere, spreading upper abdominal pain.Patients that are greater than the age of 55should also be referred to their physician assoon as possible.1

In the community setting, a patient maycome in with dyspepsia or epigastric pain, ask-ing for a recommendation on antacids, histamine2 blockers, or proton-pump inhibitors which areavailable over-the-counter (OTC). Patients mayuse these for symptomatic relief; however theseshould not be recommended for ulcer therapy. Itis very important to note that these medications

are not indicated for peptic ulcer disease asover-the-counter products. Therefore, when suspecting peptic ulcer disease, patients shouldbe referred to their physician.9

DiagnosisThere are certain conditions that mimic the

symptoms of PUD. Therefore, diseases such asmyocardial infarction, pericarditis, esophagitis,cholecystitis, pancreatitis, and irritable boweldisease should be considered when evaluating apatient for a possible ulcer.3

Endoscopy is the most accurate way to visualize the ulcer and may also allow for biopsyand cytologic study if necessary. Radiography,although it may miss up to 20% of ulcers, is oftenused to make the initial diagnosis since it ischeaper and even patients in fragile conditioncan usually tolerate it. If bleeding is suspected orif cost is not an issue, endoscopy is preferred. Inthe case of duodenal ulcers, radiographic diagnosis does not warrant a follow upendoscopy and reassessment via radiography isnot routinely done after treating the ulcer. On theother hand, gastric ulcers usually requireendoscopy to rule out malignancy or at least afollow-up radiographic assessment to provehealing after 8 to 12 weeks of treatment.

Laboratory studies are usually recommend-ed in a certain subset of patients where hyper-secretory diseases such as Zollinger-Ellisonsyndrome are suspected. Serum gastrin shouldbe measured in patients with a family history ofPUD, ulcers associated with increase calciumlevels or diarrhea, and recurrent ulcers requiringsurgery, as well as other indications as dictated by their healthcare provider.Additionally, H. pylori should be tested for viabiopsy or C-urea breath test.4

TreatmentMedications and surgery are options in the

treatment of peptic ulcer disease. Usually, medications are first line in treating ulcers, however surgery may be indicated in certainpatients with complications. Indications for

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surgery usually include complications of ulcerssuch as hemorrhage, perforation, or gastric outlet obstruction as well as intractable (untreat-able or resistant) ulcer disease.1

Duodenal ulcers can be treated with histamine-2 receptor antagonists (H2RAs) suchas ranitidine 150mg twice daily or 300mg at bed-time, famotidine 20mg twice daily or 40mg atbedtime, or cimetidine 400mg twice daily or800mg at bedtime for four to eight weeks.Duodenal and gastric ulcers can be treated withproton pump inhibitors (PPIs) for eight weeks.Typical PPI regimens include once daily treatment with omeprazole 20mg, lansoprazole15mg, rabeprazole 20mg, or pantoprazole40mg. Additionally, sucralfate is an option to usefor four weeks at a dose of 1 gram four timesdaily.2

Proton Pump Inhibitors (PPIs)As of April 2010, six proton pump inhibitors

are on the United States market for use. These include dexlansoprazole, lansoprazole, omeprazole, esomeprazole, pantoprazole, andrabeprazole. There are several GI-related indications for these agents, but we will concentrate on their use in the treatment of peptic ulcer disease. These PPIs have similarefficacy and side effect profiles while differingmainly in doses and dosing schedules.

The mechanism of action of proton pumpinhibitors is to suppress gastric acid by inhibitingthe proton pump in parietal cells. The PPIs irreversibly bind to the active H+/K+ATPasepumps leading to the inhibition of hydrogen ionsflow into the gastric lumen. The basal and meal-stimulated acid production is inhibited by PPIs.Initially, there is only a limited amount of acidproduction inhibited by PPIs; however more isinhibited once steady-state is reached after fiveto seven days of therapy. Dosing PPIs twicedaily allows for more pumps to be inhibited, leading to more rapid and complete gastric acidsuppression. Additionally, alkalinization of gastric pH leads to less pepsinogen conversionto pepsin.10

The side effect profile for PPIs is generallyminimal. Clinical studies showed that the mostcommon side effects of headache, abdominalpain, and diarrhea, were found to occur in simi-lar frequency to placebo. Additionally, there wasa concern of fundic gland polyps; however thereare no studies that advise stopping PPIs in thiscase. Other concerns associated with PPI useinclude increased incidence of gastric carci-noids, vitamin B12 deficiency, pneumonia,Clostridium difficile infections, and an increase inhip fractures. The carcinoids and vitamin B12deficiency have not been proven to be true; concern of pneumonia is difficult to substantiatesince the study included many patients with multiple co-morbidities; and the C. difficilecorrelation was seen in case-control studies butthe mechanism is not clear. Additionally, theincreases in hip fractures have been shown inseveral studies where other confounders weretaken into account and therefore, although thereare no guidelines that discourage long term useof PPIs in patients, the association between longterm PPI use and hip fractures is possible. Onthe other hand, an observational study did notfind any of the aforementioned side effects forthe 11 years that 230 patients were on PPI therapy.10

There are six PPIs on the market currentlyand some are available without a prescription.Each PPI differs in the availability of dosageforms, strength, dosing schedule, and FDA-approved indications, which will not be discussed in this review.11

• Dexlansoprazole (Dexilant®) is the newest PPI available. There is no dosingsuggested for the treatment of peptic ulcerdisease.12

• Esomeprazole (Nexium®) is available ascapsules, oral suspension, and for intravenous (IV) use. The dosing for H. pylori eradication is 40mg daily in thetriple or quadruple therapy regimen (refer tothe section on H. pylori eradication). Thedosing for the prevention of NSAID-inducedulcers is 20 to 40mg daily for up to six

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months and 40mg twice daily (maximum of240mg/daily) may be used in pathologichypersecretory conditions. The IV dosing is80mg twice daily for pathologic hypersecretory conditions. The maximumdose of esomeprazole is 20mg daily forpatients with severe hepatic impairment. Itshould be taken one hour before meals andthe granules from the capsules can bemixed with applesauce or given through thenasogastric (NG) tube. The suspension canbe given through the NG tube as well.11

• Lansoprazole (Prevacid®) is available over-the-counter, prescription, and generic. It isavailable in 15mg and 30mg strengths asdelayed release granules for suspension,delayed release capsules, and delayedrelease orally disintegrating tablets (ODT). It is also available in 30mg powder for injection. The OTC formulation is only available as a 15mg delayed release tablet.The prescription dosing for the prevention ofNSAID-induced ulcers is 15mg daily for upto three months and 30 mg daily up to eightweeks for the treatment of NSAID inducedulcers; the dose should be reduced inpatients with hepatic impairment. The granules from the capsules and the ODTcan be given through an NG tube; howeverunlike esomeprazole, the suspension shouldnot be given this way. Additionally, applesauce, Ensure pudding, cottagecheese, yogurt, strained pears, apple,orange, or tomato juice can be used to mixthe granules from the capsules just so longas it is taken immediately.11

• Omeprazole is also available OTC, prescription, and generic. The Zegerid® andZegerid® OTC formulations containomeprazole and sodium bicarbonate; whilethe Prilosec® formulation contains onlyomeprazole. Zegerid® is available onlyunder the brand name in 20mg and 40mgcapsules (with 1,100mg of sodium bicarbon-ate) and powder for suspension (with1,680mg of sodium bicarbonate); the OTC formulation contains omeprazole

20 mg/sodium bicarbonate 1,100 mg capsules. Since the bicarbonate in each ofthe capsules is the same, two 20mg capsules is not the same as one 40mg capsule. The sodium bicarbonate used inthis formulation is for the protection of omeprazole from the acidic nature of thestomach thereby allowing for its absorption.It is dosed at 20mg daily for four weeks forthe treatment of duodenal ulcers and at40mg daily for four to eight weeks forbenign gastric ulcers, taken on an emptystomach, one hour prior to meals. The preventive dose for bleeding in critically illpatients is 40mg daily after giving 40mgtwice daily, spaced by 6 to 8 hours on dayone. Unlike the other capsules, the granulescan not be removed; however the powderfor suspension can be used via NG tube.On the other hand, omeprazole is availablein 10mg, 20mg, and 40mg capsules (cansprinkle contents into applesauce) and2.5mg and 10mg suspension (can be giventhrough the NG tube); the OTC formulationcontains 20mg of omeprazole. The dosingfor duodenal ulcers is 20mg daily for fourweeks (repeat for an additional four weeks ifnecessary) and 40mg daily for four to eightweeks for gastric ulcers. The dosing forpathologic hypersecretion is 60mg daily witha maximum of 360mg/day.11

• Pantoprazole (Protonix®) is dosed at 40mgtwice daily or 80mg every 12 hours (maximum of 240mg/day) for pathologichypersecretory conditions. It is availablegenerically in 20mg and 40mg tablets, 40mgsuspension, and 40mg injection. The suspension should be taken 30 minutesprior to meals and may be used via NGtube.11

• Rabeprazole (Aciphex®) is available in20mg tablets and dosed at 20mg daily forfour to eight weeks to treat duodenal ulcers and 60mg daily for pathologic hypersecretory conditions with a maximumof 120mg/day.11

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Histamine 2 Receptor Antagonist(H2RA)13

There are four available H2RAs: cimetidine,famotidine, nizatidine, and ranitidine. They areindicated for the treatment of active duodenaland gastric ulcers as well as maintenance therapy for duodenal ulcers. There is a 70 to80% rate of healing in duodenal ulcer after fourweeks and 87 to 94% after eight weeks. EachH2RA is comparable for the treatment of ulcersand may be taken as one dose at bedtime ordivided into multiple doses. Multiple doses ispreferred in patients who experience daytimesymptoms. Smokers require higher doses andmay need to be treated for a longer period oftime; whereas patients with moderate to severerenal failure should have a dose reduction or anincreased duration between doses. Generallythe side effect profile is minimal; however, central nervous system related side effectsrarely occur in patients with renal failure due tomedication accumulation. Another rare sideeffect implicated in H2RA therapy is thrombocy-topenia. Of the four H2RAs, cimetidine has themost drug interactions due to its inhibition of several CYP450 isoenzymes.2

• Cimetidine (Tagamet®) is dosed at 400mgtwice daily (or 800mg at bedtime) to a maximum of 1600mg/day for duodenalulcers and 300mg four times daily for gastric ulcers; the maintenance dose is400mg at bedtime.13

• Famotidine (Pepcid®) is dosed at 40mg atbedtime for gastric ulcers; 20mg twice dailyfor active duodenal ulcers and then oncedaily for maintenance therapy.13

• Nizatidine (Axid®) is dosed at 300mg atbedtime for duodenal ulcers or 150mg twicedaily for duodenal and gastric ulcers, using150mg at bedtime for the maintenance therapy.13

• Ranitidine (Zantac®) is dosed the same asnizatidine.13

SucralfateSucralfate, being viscous in nature and

having a negative charge, works by binding toduodenal and gastric ulcers and to gastric erosions. It binds to gastric mucosa, creating abarrier from the acid, as well as buffers the acid,inhibits pepsin, and adsorbs bile salts.14 Thetreatment dose for duodenal or gastric ulcers is1 gram four times daily or 2 grams twice dailyand the maintenance dose is 1 to 2 grams twice daily or 1 gram four times daily.2 This medication is not commonly used anymore,most probably because of the amount and frequency of dosing, as well as the need to betaken on an empty stomach. Side effects include constipation, nausea, dry mouth, metallic taste in the mouth, as well as rare occurrence of seizures and hypophosphatemia.Sucralfate should be taken two hours after medications such as fluoroquinolones,phenytoin, digoxin, theophylline, amitriptyline,warfarin, and ketoconazole.2

Bismuth Bismuth subsalicylate is thought to heal

ulcers by an antibacterial and local gastro-protective effect as well as by stimulatingprostaglandins. Adverse effects include blackstool or a hairy tongue. This is not considered to be a first line agent to treat peptic ulcers.16

AntacidsThe mechanism of action of antacids are to

neutralize gastric acid, inhibit pepsin, and bindbile acids. Aluminum containing antacids havethe additional mechanism of increasing mucosaldefense and suppressing H. pylori. Antacidsusually contain aluminum or magnesium andcause more immediate relief for symptoms ofdyspepsia. However, they have many drug interactions which may decrease absorption ofcertain medications. Although they may be usedin patients with peptic ulcer disease, they are notconsidered first line therapy.

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H. Pylori EradicationWhen a patient with peptic ulcer disease

tests positive for H. pylori, first-line eradicationtherapy is recommended with a triple therapycombination of a PPI, clarithromycin, and amoxicillin, or metronidazole.15 The worldwiderate of eradication is usually 70 to 85 percent.15

There are several different combinations utilizedto eradicate H. pylori. In general, the duration ofeach combination is 10 to 14 days. Althoughsome of the PPIs or bismuth-based regimenshave FDA-approved indications, studies haveshown similar efficacy among all of them.15,16

Amoxicillin is the preferred antibiotic in combination with clarithromycin; however inpatients with penicillin allergies, metronidazolecan be substituted. This substitution is recom-mended to occur only in patients that can nottake penicillins because if the metronidazoletherapy is ineffective, salvage therapy is foundalso to not be effective. Quadruple therapy usinga PPI, bismuth, tetracycline, and metronidazolefor 10 to 14 days is considered to be either analternative first line therapy or a salvage therapyto patients failing clarithomycin based therapy.15

Another salvage therapy option is using levofloxacin in conjunction with a PPI and amoxicillin.15

Table 1 outlines the various combinationsavailable (refer to Table 1 on pages 12-13).Some of these combinations may also be available in prepackaged brand name formulations. It is important to note that Helidac®and Pylera® do not contain the PPI and therefore would require a separate prescriptionfor proper eradication. Since there are severalcombinations available to eradicate H. pylori,choosing a regimen should take the followingfactors into consideration: eradication rate(>80% is preferred), cost, insurance, formulary,dosing schedule, and side effects.16

There is evidence linking H. pylori as a causeof gastric cancer, one of the most common cancers worldwide. It is important to note that theincidence varies greatly by geographic region.Eradication of H. pylori with antibiotics and PPI

therapy is shown to decrease the incidence ofgastric cancer.17 However, there was also another study that did not show a significantdecrease in gastric cancer with H. pylorieradication in a population that has the secondhighest incidence of gastric cancer. This studynoted that further studies evaluating early eradication of H. pylori with vigilant follow-updata are needed.18

Prevention of NSAID-Related UlcerComplications

One of the most common causes of ulcers isthe use of NSAIDs. Clinical practice guidelinesfor the prevention of NSAID-related ulcers havebeen created to provide recommendations tohealth care providers using scientific data fromstudies.7

Prevention of NSAID-related pepticulceration and mucosal injury is commonly practiced utilizing one of two methods. The firstmethod is to concurrently prescribe a PPI, high-dose (double dose) histamine-2-receptorantagonist (H2RA) or misoprostol. The secondmethod is to use a COX-2 inhibitor.

Misoprostol is a synthetic prostaglandin E1analog and was the first agent approved for theprevention of NSAID-related ulcers. It works byinhibiting gastric acid (basal, nocturnal, and stim-uli-induced) as well as by increasing bicarbonateand mucus production.19 Meta-analysis studieshave shown that misoprostol is statistically morelikely to prevent NSAID-induced ulcers thanplacebo or H2RA and similarly to lansoprazole.Additionally, misoprostol 200mcg four times dailywas evaluated in a large, randomized, placebocontrolled study and it showed a 40% decreasein serious upper GI complications. The FDA-approved dose is 200mcg four times daily withfood, however, doses of 400-600mcg/day havealso shown a significant decrease in ulcerationcompared to placebo.20 Although it is gastroin-testinal protective, the main limitation of miso-prostol is the occurrence of side effects. Themain side effects of misoprostol include diarrhea,abdominal pain, nausea, bloating, and fullness.19

_continued on page 14.

13


Tabl

e 1:

Com

bina

tion

Med

icat

ions

for t

he E

radi

catio

n of

H. P

ylor

i11,1

3,16

Omeprazole

Esomeprazole

Lansoprazole

Pantoprazole

Rabeprazole

Clarithromycin

Amoxicillin

Metronidazole

Tetracycline

Bismuth Subsalicylate

Tinidazole

Rifampin

Levofloxacin

10 to

14

days

40

mg

500m

g10

00m

g FD

A -a

ppro

ved

daily

B

IDB

ID

14 d

ays

20m

g50

0mg

500m

g B

ID o

rB

IDB

ID

40m

g da

ily

10-1

4 da

ys30

mg

BID

500m

g10

00m

gFD

A –a

ppro

ved

BID

BID

Avai

labl

e as

Pre

vPac

®

14 d

ays

30m

g B

ID50

0mg

BID

500m

g B

ID

10 d

ays

20m

g B

ID50

0mg

BID

1000

mg

FDA

-app

rove

dB

ID

14 d

ays

20m

g B

ID50

0mg

BID

500m

g B

ID

14 d

ays

40m

g B

ID50

0mg

BID

1000

mg

BID

14 d

ays

40m

g B

ID50

0mg

BID

500m

g B

ID

14 d

ays

20m

g B

ID50

0mg

BID

1000

mg

BID

14 d

ays

20m

g B

ID50

0mg

BID

500m

g B

ID

10 to

14

days

Eso

mep

razo

le 2

0mg

BID

OR

40m

g da

ily O

R25

0mg

500m

g52

5mg

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mut

h/ M

etro

nida

zole

/La

nsop

razo

le 3

0mg

BID

OR

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epra

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20m

g BI

D O

Rfo

ur ti

mes

four

tim

esfo

ur ti

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Te

tracy

clin

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aila

ble

Pan

topr

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mg

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OR

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epra

zole

20m

g B

IDda

ilyda

ilyda

ily

as H

elid

ac®

Com

bina

tion




Tabl

e 1:

Com

bina

tion

Med

icat

ions

for t

he E

radi

catio

n of

H. P

ylor

i11,1

3,16

C

ON

TIN

UE

D

Omeprazole

Esomeprazole

Lansoprazole

Pantoprazole

Rabeprazole

Clarithromycin

Amoxicillin

Metronidazole

Tetracycline

Bismuth Subsalicylate

Tinidazole

Rifampin

Levofloxacin

10 to

14

days

with

aFa

mot

idin

e 40

mg

daily

OR

Niz

atid

ine

300m

g da

ily O

R25

0mg

500m

g52

5mg

H2R

A an

dR

aniti

dine

150

mg

twic

e da

ilyfo

ur ti

mes

four

tim

esfo

ur ti

mes

B

ism

uth/

Met

roni

dazo

le/

(Ran

itidi

ne is

FD

A-a

ppro

ved

in th

is c

ombi

natio

n)

daily

daily

daily

Tetra

cycl

ine

avai

labl

e as

Hel

idac

®

10 d

ays;

20m

g B

ID50

0mg

1000

mg

500m

g50

0mg

500m

g

not c

onsi

dere

dB

ID d

ays

BID

day

s B

ID d

ays

BID

day

sB

ID d

ays

1st l

ine

ther

apy

6 to

10

1 to

56

to 1

06

to 1

06

to 1

0

14 d

ays;

if a

pat

ient

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30m

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ic to

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ree

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Tetra

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tda

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r th

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adic

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are

14 d

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then

20m

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day

s da

ily fo

r 14

day

s

10 to

14

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whe

nE

som

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zole

20m

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ID O

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15


The incidence of diarrhea is between 14 to 40%and 13 to 20% experience abdominal pain.19

Additionally, spotting, cramps, hypermenorrhea,menstrual disorder, and dysmenorrhea occurredin women. Misoprostol is pregnancy category Xand therefore is contraindicated in pregnantwomen (refer to tables 2 and 3).19

PPISeveral randomized clinical trials have been

done to evaluate the role of PPIs in preventingNSAID-induced peptic ulcers. Two of the majorclinical trials compared omeprazole to placebo,misoprostol, and ranitidine in patients with ulcersor erosions. The results showed a significantdecrease in NSAID-related ulcers in the omeprazole group when compared to ranitidine.In comparison to misoprostol, omeprazole had ahigher prevention rate of duodenal ulcers but the same prevention rate of gastric ulcers.7

High-dose H2RA Single-dose H2RAs do not provide a

reduction in the risk of NSAID-induced gastriculcers. On the other hand, double-dose H2RAsare effective in reducing the risk and may be amore cost-effective alternative for some patients.Prescribing an H2RA in all patients with a low toaverage risk of developing ulcers while onNSAID therapy was a strategy suggested by aneconomic analysis study.7

COX-2 InhibitorsMedications such as celecoxib (Celebrex®)

and rofecoxib (Vioxx®) were developed todecrease inflammation in musculoskeletal tissuewithout causing gastrointestinal mucosal

Risk Factor Definition

A Controlled studies in women fail to show a risk to the fetus

B 1) Animal-reproduction studies fail to show a fetal risk but no controlled studies in women are available

2) An adverse effect seen in animal reproduction studies but not confirmed in controlled studies in women

C 1) Animal-reproduction studies show an adverse effect on the fetus and no controlled studies in women are available

2) There are no studies in animals or women

D • Evidence exists of human fetal risk• Benefit of medication may outweigh risk

X • Evidence exists of fetal risk in studies of animals or humans and/or human experience

• Benefit of medication does not outweigh risk• Use in pregnancy is contraindicated

Table 2: Pregnancy Risk Factor Definition22

Drug CategoryCimetidine BFamotidine BLansoprazole BMisoprostol XNizatidine BOmeprazole CPantoprazole BRabeprazole BRanitidine BSucralfate B

Table 3: Pregnancy Risk Categorization ofMedications for PUD19, 23

16


damage by selectively inhibiting COX-2. Threestudies, CLASS, VIGOR, and TARGET com-pared various COX-2 inhibitors to traditionalNSAIDs in patients with arthritis.10 In the firststudy, results showed a significant decrease inulcer complications in the celecoxib group at sixmonths only after the data was adjusted toexclude patients taking aspirin. At one year inthis study, results indicated no differencebetween any of the groups. In the second study,naproxen was compared to rofecoxib (which hassince been voluntarily taken off the market) anda significant decrease in ulcers was noted in therofecoxib group. The third study looked at lumiracoxib (a COX-2 inhibitor that was neverapproved in the United States and taken off the approved list in other countries because of hepatotoxicity) which showed a decrease in gastric complications. The Cochrane databasealso reviewed COX-2 inhibitors and concludedthat patients taking COX-2 inhibitors have significantly less gastroduodenal ulcers, complications, and withdrawals to therapybecause of gastrointestinal symptoms.7

In summary, full dose misoprostol, PPIs, andthe use of COX-2 inhibitors instead of traditionalNSAIDs are effective in preventing ulcers andulcer complications in patients taking NSAIDs.High-dose H2RAs are effective compared toplacebo but not as effective as PPIs. In choosinga preventive therapy, it is important to considerthe limitations with each of these preventivestrategies. The main limitation of using miso-prostol is its GI side effects. Cost of the PPIs andcelecoxib may be a consideration for somepatients. Another limitation with celecoxib is thatpatients concurrently taking low dose aspirin,who do not get the benefit of the decrease ingastrointestinal events, are at risk of cardiovas-cular events. In general, the lowest doses ofNSAIDs should be utilized.7

The clinical practice guidelines recommendrisk stratification by counting the number of riskfactors a patient has of developing NSAID-induced gastrointestinal injury. In this example ofrisk stratification, the guidelines state low risk

means no risk factors, moderate risk means 1 to2 risk factors, and high risk means either historyor a previous complication ulcer or more than 2risk factors. The next step is to consider the cardiovascular risk since NSAIDs have beenassociated with an increased incidence of cardiovascular (CV) events. Risk factors for CVdisease include prior history of CV event, diabetes, hypertension, hyperlipidemia, and obesity. After determining the risk factors forgastrointestinal and CV events, the guidelineshave recommended a prevention strategy foreach of the groups. In patients with a low gastrointestinal risk and low CV risk, NSAIDs atlowest effective dose should be prescribed. Inpatients with moderate gastrointestinal risk andlow CV risk, use an NSAID with either a PPI ormisoprostol. Patients with a high gastrointestinalrisk should either be given alternative therapy ora COX-2 inhibitor with a PPI or misoprostol. Inpatients with high CV risk but low or moderate GIrisk, naproxen with a PPI or misoprostol is recommended. Patients with high GI and CVrisk, NSAIDs and COX-2 inhibitors should beavoided.7

PPI Use in Pregnancy21

The first PPI, omeprazole, has several studies that evaluated its safety during pregnancy. In one study, 113 women exposed toomeprazole during pregnancy were compared totwo control groups. One control was a disease-paired group using histamine 2 blockers and the other group was healthy women given nonteratogenic (medications not causing birthdefects) medications. The authors found thatthere was no significant difference in the occurrence of major malformations, sponta-neous abortions, pre-term deliveries, caesareansection, and neonatal health problems. Anotherstudy, also conducted by Motherisk, showed thatthe use of omeprazole in 534 women thatshowed no increase in the risk of malformations.Additionally, the Swedish Medical Birth Registry found that rates of birth weight, congenital malformations, perinatal death, andlow Apgar scores of 955 infants exposed to

17


omeprazole while the mothers were pregnant(including a majority that were exposed duringtheir first trimester), were comparable to the general Swedish population.

Pantoprazole and lansoprazole, in addition toomeprazole, were also compared to a controlgroup in another prospective study (a study thatfollows patients forward in time). In this study, theomeprazole group had 295 pregnant women, thelansoprazole group had 62, and the pantopra-zole group had 53. The rate of major congenitalmalformations was not significantly different inany of the three PPI groups when compared tothe control group (3.6% in the omeprazole group,3.8% in the pantoprazole group, 3.9% in the lansoprazole group, and 3.8% in the controlgroup). In general, PPIs may be used in pregnancy, however, should only be done sounder doctor’s orders.

Complications2

Hemorrhage, perforation, and gastric outletobstruction are complications that may occurwith peptic ulcer disease. It occurs in about 25%of patients with peptic ulcer disease with uppergastrointestinal bleeding and is the most common cause of death because of the disease.Symptoms of upper gastrointestinal bleedinginclude bright red or coffee ground blood in thestool, melena, fatigue, anemia, orthostatichypotension, and syncope; however, manypatients do not have any symptoms of the ulcer.Another complication is perforation of the duodenum wall or antral wall which may lead toperitonitis. Symptoms of perforation includeextreme pain in the abdomen with fever andhypotension if the patient becomes septic. Itrequires emergency surgery and the mortality(death) rate in older patients is 30 to 50%. Lastly,gastric obstruction resulting from pyloric stenosismay present as vomiting, fullness, weight loss,dehydration, or metabolic alkalosis and usuallyrequires surgery.

CONCLUSIONPeptic ulcer disease is a fairly common

disease inflicting both men and women. It maybe treated in the outpatient setting; however,there is the possibility of complications and evendeath if the disease progresses without recognition and treatment. The main causes areH. pylori and non-steroidal anti-inflammatorydrug use. In the case of H. pylori, medicationsaimed at healing the ulcer and eradicating theinfection are used in combination while in thecase of NSAIDs, medications are give to heal the ulcer and the offending agent is usually discontinued. Patients should be closely monitored for the healing of the ulcer and theprevention of reoccurrences. ■

18


REFERENCES1. Ramakrishnan K, Salinas RC. Peptic ulcer

disease. Am Fam Physician [Internet]. 2007 Oct 1;76(7):1005-12.

2. Berardi RR, Welage LS. Peptic ulcer disease. In:Pharmacotherapy: A Pathophysiologic Approach,Dipiro J (Ed).

3. Soll A. Overview of peptic ulcer: epidemiology and major causes. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2009.

4. Halter F. Pathophysiology of peptic ulcer disease. In: Hollander D, Tytgat GNJ, editors. Sucralfate: From Basic Science to the Bedside.NY: Plenum Press;1995.

5. Pizzo de Castro MR, Matsuo T, Varges Nunes SO. Clinical characteristics and quality of life of smokers at a referral center for smoking cessation. J Bras Pneumol. 2010;36(1):67-74.

6. Dorer MS, Talarico S, Salama NR. Helicobacter pylori‘s unconventional role in health and disease. PLoS Pathogens [serial online] 2009. Available from URL: http://www.ploscollections.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000544[accessed March 1, 2010].

7. Lanza FL, Chan FKL, Quigley EM, et al. Guidelines for prevention of NSAID-related ulcercomplications. Am J Gastroenterol.2009;104:728-738.

8. Sung J, Lau JY, Ching JC, Wu Y, et al. Continuation of Low-Dose Aspirin Therapy in Peptic Ulcer Bleeding. A Randomized Trial. Ann Intern Med. 2010;152(1-9).

9. Pray WS. Nonprescription Products Therapeutics. Binghamton, NY: Pharmaceutical Products Press, August 2003.

10. Katz PO, Zavala S. Proton Pump Inhibitors in the Management of GERD. J Gastrointestinal Surge. 2010:14(Suppl 1):S62–S66.

11. Comparison of proton pump inhibitors. Pharmacist’s Letter/Prescriber’s Letter2009;25(3):250304. (Full update January 2010)

12. Dexilant [package insert]. Deerfield, IL: Takeda Pharmaceuticals, Inc; 2010.

13. Histamine H2 blocker oral dose comparison. Pharmacist’s Letter/Prescriber’s Letter2009;25(8):250801.

14. Nagashima R. Mechanism of action of sucralfate. J Clin Gastroenterol.1981;3(Suppl 2):117-27.

15. Chey WD, Wong B. American College of Gastroenterology Guideline on the Management of Helicobacter pylori Infection. Am J Gastroenterol 2007;102:1808-1825.

16. H. pylori treatment regimens. Pharmacist’s Letter/Prescriber’s Letter 2007;23(11):231113.

17. Konturek PC, Konturek SJ, Brzozowski T. Helicobacter pylori infection in gastric cancerogenesis. J Physiol Pharmacol.2009 Sep;60(3):3-21

18. Mabe K, Takahashi M, Oizumi H, Tsukuma H, Shibata A, Fukase K, Matsuda T, Takeda H, Kawata S. Does Helicobacter pylori eradication therapy for peptic ulcer prevent gastric cancer? World J Gastroenterol. 2009;15(34):4290-4297 Available from: URL: http://www.wjgnet.com/1007-9327/15/4290.aspDOI:http://dx.doi.org/10.3748/wjg.15.4290. [accessed March 1, 2010].

19. Cytotec [package insert]. New York, NY: Pfizer; 2009.

20. Park SH, Cho CS, Lee OY, Jun JB, et al. Comparison of prevention of NSAID-induced gastrointestinal complications by rebamipide andmisoprostol: a randomized multicenter, controlled trial-STORM study. J. Clin. Biochem Nutr. 2007;40:148-155.

21. Nava-Ocampo AA. Velazquez-Armenta EY. Han JY. Koren G. Motherisk Update. Canadian Family Physician. 2006;52:853-854.

22. “Pregnancy and Medicines” U.S. Department of Health and Human Services, Office on Women’sHealth http://www.womenshealth.gov/faq/pregnancy-medicines.cfm [accessed September 7, 2010].

23. Vanderhoff BT, Tahboub RM. Proton pump inhibitors: an update. Am Fam Physician.2002 Jul15;66(2):273-281.

19


VOLUME 15 NO. 4 PEPTIC ULCER DISEASESELF-ASSESSMENT QUESTIONS 1 — 20

1. What is/are the most common cause(s) of peptic ulcer disease?A. H. pyloriB. NSAIDsC. FoodD. A and B

2. Which of the following is a medication that may cause an ulcer?A. NaproxenB. AcetaminophenC. SucralfateD. Omeprazole

3. Which of the following has a major role in the pathogenesis of peptic ulcer disease?A. PepsinB. AntihistamineC. BicarbonateD. Mucosal blood flow

4. What may increase the risk of developing peptic ulcer disease?A. AnorexiaB. AlcoholC. Smoking cigarettesD. Soda

5. A patient is currently taking warfarin andis to be started on sucralfate. Which of the following is the BEST counseling point for a pharmacist to give to this patient?A. There is no drug-drug interaction and

therefore can be taken together at the same time.

B. Warfarin and sucralfate can not be taken together. We will call the doctor to change one of your medications.

C. Sucralfate should be taken 2 hours after warfarin

D. Warfarin should be taken 1 hour after sucralfate.

6. H. Pylori may cause peptic ulcer disease by inducing:A. pepsinB. hydrochloric acidC. inflammationD. viral infections

7. Even at low dose, ____________ is associated with an increased risk of developing peptic ulcer disease.A. hydrocodoneB. aspirinC. acetaminophenD. pseudoephedrine

8. Which of the following is a symptom of peptic ulcer disease?A. NauseaB. Epigastric painC. VomitingD. All of the above

20


9. If a patient complains of dyspepsia and adds he/ she may have an ulcer, the patient should be:A. referred to the physicianB. referred to the emergency roomC. shown to the stomach pain relief aisleD. advised to take acetaminophen

10. PPI stands for:A. pantoprazole pump inactivatorB. proton pump inhibitorC. proton pump inactivatorD. prilosec prevacid inhibitor

11. The gold standard for diagnosing peptic ulcer disease is via:A. bronchoscopyB. ultrasoundC. endoscopyD. surgery

12. Rabeprazole is an example of a/an:A. H2RAB. PPIC. NSAIDD. Antacid

13. Which of the following is superior in treating PUD?A. RabeprazoleB. OmeprazoleC. LansoprazoleD. All have the same efficacy

14. Triple therapy to treat H. pylori includes:A. antibiotics and H2RAB. antibiotics and PPIC. H2RA and PPID. A and B

15. Which of the following is an example of an H2RA?A. RanitidineB. SucralfateC. OmeprazoleD. Azithromycin

16. Which of the following can be given with an NSAID to prevent ulcers?A. MisoprostolB. AzithromycinC. OmeprazoleD. A or C

17. Which of the following can be given for inflammation instead of an NSAID to reduce the likelihood of getting an ulcer?A. NaproxenB. IbuprofenC. MeloxicamD. Celecoxib

18. Which of the following is a complication of an ulcer which may require surgery?A. PerforationB. HemorrhageC. Gastric outlet obstruction D. All of the above

19. What is the consensus of PPI use in pregnancy?A. PPIs are absolutely contraindicatedB. PPIs may be used freelyC. PPIs may be considered if benefit

outweighs riskD. PPIs are teratogenic

20. Which of the following is/are (an) option(s) to treat ulcers?A. NaproxenB. SurgeryC. CimetidineD. B or C

21


PEPTIC ULCER DISEASE - pharmacytechtopics.com · 10/31/2012 · Describe the pathophysiology of peptic ulcer disease. 2. List the risk factors for developing peptic ulcer disease

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