Peptic Ulcer Disease

DefinitionEtiologyEpidemiologyPathophysiologyClinical Manifestation
WorkupRN ManagementMedsDiagnosis and GoalsInterventionAlertsRefs

Erosion of the gastrointestinal mucosa extending through muscularis mucosa, involving the stomach (gastric ulcer), and duodenum (duodenal ulcer).


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Common causes:

  • Helicobacter pylori (H. pylori) infection
  • Nonsteroidal anti-inflammatory drugs (NSAIDs)

Less common causes:

  • Other drugs may include steroids, bisphosphonates
  • Carcinoid syndrome
  • Post-gastric surgery
  • Chronic renal failure
  • Radiation/chemotherapy
  • Zollinger-Ellison syndrome
  • Crohn's disease
  • Ischemia, usually related to crack cocaine use

Risk factors:

  • Smoking/stress
  • Diabetes mellitus
  • Cirrhosis


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  • Annual incidence of PUD ranges from 0.1-0.3%
  • Incidence increases with age
  • Incidence in H. pylori-infected individuals is ~1% per year
  • 70% of ulcers occur between ages 25 and 64 years
  • No predilection by gender
  • First-degree relatives of patients with duodenal ulcer (DU) have a threefold increase in the prevalence of DU but not gastric ulcer (GU)
  • Lifetime prevalence is 8-14%; 20% higher in H. pylori positive subjects
  • Mortality rate is approximately 1 death per 100,000 cases
  • Hospitalization rate is 30 patients per 100,000 cases


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Parietal cells of stomach produce acid and decrease pH, which in turn causes release of somatostatins leading to inhibition of acid secretion (by negative feedback control)..

Within the acidic environment of the stomach, the mucosa is protected by several mechanisms as follows:

  • Production of mucus and HCO3 where mucus serves as a barrier to acid diffusion
  • Epithelial cells remove excess H+ ions and prevent back diffusion
  • Mucosal blood flow removes excess acid
  • Growth factors and prostaglandins are shown to have protective effects

Factors that interfere with these mucosal defenses (particularly NSAIDs and Helicobacter pylori infection) predispose to gastritis and peptic ulcer disease.

NSAIDs cause mucosal inflammation and ulcer formation by:

  • Inhibiting prostaglandin production by blocking enzyme cyclooxgenase (COX)
  • Reduce gastric blood flow causing decrease cell repair and replication
  • They are weak acids, diffuse freely across the mucus membrane, liberating H+ ions leading to cellular damage

Helicobacter pylori: Interferes with mucosal physiology mechanisms include

  • Increase acid secretion (combination of increase in acid secretions and decrease in duodenal bicarb secretion resulting low pH)
  • Gastric metaplasia (promoted by increased acid secretion)
  • Alters immune responses leading to persistent colonization
  • H. pylori colonization in duodenum induces inflammation and reduces bicarb secretion thus promoting ulcer formation
  • Diminishes mucosal defense mechanism


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Clinical Manifestations:

General symptoms:

  • Epigastric pain
  • Dyspepsia
  • ± Nausea/vomiting
  • Symptom free periods (months to years), alternate with the symptomatic periods

Other less common symptoms/complications:

  • Hematemesis
  • Melena
  • Weight loss
  • Anorexia
  • Syncope

GU: Recurrent burning or gnawing pain in the epigastrium (not related to food), heartburn, early satiety and radiation of pain to the xiphisternum.

DU: Consistent pain, which may awake the patient in the night, related with food (subsides in 50% with food intake, but recur after 2-3 hrs).

1-b-Black-Light box-PU-Clinical Presentation-Comparison


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Workup and Diagnosis:


Health history:

  • Medication usage
  • Heartburn
  • Weight loss
  • Black, tarry stools - melena
  • Anemia
  • Epigastric tenderness


History of pain includes:

  • Intensity
  • Location
  • Nature of pain (burning, squeezing)
  • Radiations
  • Associated symptoms

Attention to abnormal laboratory values, e.g. HgB, LFTs, electrolytes, amylase, lipase, cardiac biomarkers



Some epigastric tenderness may or may not be present.

Initial Lab Tests:

  • CBC
  • Serum amylase and lipase
  • Liver function test
  • Cardiac enzymes: Rule out myocardial ischemia in acute presentation
  • Helicobacter pylori serology
  • Serum gastrin
  • Gastric fluid analysis



Upper gastrointestinal radiography series:

  • Indicated when endoscopy is unsuitable or not feasible
  • Relatively low sensitivity and specificity
  • Avoid in the patient with upper GI bleeding

1-Black-Light box-PU-Investigation and workup-Benign versus Malignant lesions on x-rays


Esophagogastroduodenoscopy (endoscopy):

Most reliable diagnostic test for PUD

Indications for endoscopy include:

  • Patient >50 years with new-onset dyspepsia
  • Symptoms of bleeding, weight loss, dysphagia
  • Refractory or persistent abdominal pain
  • Suspicion of upper GI abnormality (mass, stricture, ulcers etc.)
  • Diagnosis of an H. pylori infection when non-invasive testing is not possible

2-Black-Light box-PU-Investigation and workup-Benign versus Malignant lesions on endoscopy


Indications and diagnostics for screening H. pylori infections in patients with dyspepsia


  • History of dyspepsia
  • Active or uncomplicated peptic ulcer disease
  • Gastric MALT (mucosa associated lymphoid tissue) lymphoma
  • Recent bleeding in PUD patients
  • Patients who are first degree relatives of gastric cancer patients
  • Patients with idiopathic thrombocytopenic purpura (ITP)
  • Patients with otherwise unexplained iron deficiency anemia

Noninvasive diagnostics:

  • Serology: ELISA techniques detect IgG antibodies (sensitivity ~60-90%)
  • Urea breath test (UBT): Sensitivity and specificity is about >90%
    • Discontinue proton pump inhibitors or H2 receptor antagonists, antibiotics and bismuth 4 weeks before a test based on H. pylori urease production
  • Stool antigen test (SAT): Sensitivity 91% and specificity 93%

Invasive diagnostics:


  • Biopsy (gold standard): 95% sensitive / 100% specific / results in 24 hrs
  • Rapid urease test: 95% sensitive / 95% specific / results in 1 hr

Additional Biopsy consideration and sample evaluation:

  • Brush cytology: Considered in patients with bleeding disorders; where biopsies are considered undesirable
  • Histology helps in distinguishing inflammation, metaplasia and MALT
  • Polymerase Chain reaction (PCR) used only when ordinary culture cannot be done

Confirmation of eradication should be strongly considered and assessed through noninvasive tests (stool and breath tests).


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RN/Medical Management:

Peptic ulcer disease is treated according to its cause:

  • H. pylori associated ulcer
  • NSAIDs associated ulcers
  • Refractory ulcers


Goal is to relieve dyspepsia, promote healing and cure infection.

Uncomplicated ulcers are treated for 10-14 days, provided ulcer is <1cm and dyspepsia resolves; treatment options are as follows:

1st Line Therapy (eradication rates 70-85%):

Combination of:


  • Pantoprazole 40 mg PO BID, omeprazole 20 mg PO BID or rabeprazole 20 mg PO BID or lansoprazole 30 mg PO BID are few examples


  • Clarithromycin 500 mg PO BID


  • Amoxicillin 1 gm PO BID (if penicillin allergic give metronidazole 500 mg PO BID)

2nd Line Therapy (eradication rates 75-90%):

  • PPIs PO BID (as mentioned above) PLUS
  • Bismuth subsalicylate 2 tabs PO QID PLUS
  • Tetracycline 500 mg PO QID PLUS
  • Metronidazole 250 mg PO QID

OR the combine formulation of:

  • Pylera 3 capsules PO QID which is a combination of (Bismuth + Tetracycline + Metronidazole)

3rd Line Therapy (reports of eradication rates vary):

  • PPIs PO twice daily (as mentioned above) PLUS
  • Day 1-5: Amoxicillin 1 gm PO daily PLUS
  • Day 6-10: Clarithromycin 500 mg and metronidazole 500 mg, both twice daily

Complicated ulcers or ulcers >1cm: Antisecretory agent should be given for additional 2-4wks in duodenal ulcers and 4-6wks in gastric ulcers.

Note: Confirm eradication after >4 wks of completion of therapy by invasive or non-invasive methods.


Active ulcers: Are to be treated by discontinuing offending agents if possible.

Consider other causes like Zollinger-Ellison syndrome and gastric malignancy.

Treatment options:


  • Pantoprazole 40 mg PO BID, omperazole 20 mg PO BID or rabeprazole 20 mg PO BID or lansoprazole 30 mg PO BID are few examples
  • Duodenal ulcers (uncomplicated) treated for 4 weeks
  • Gastric ulcers (uncomplicated) treated for 8 weeks
  • For complicated ulcers PPIs are preferred drugs

H2 receptor antagonists:

Uncomplicated duodenal ulcers:

  • Cimetidine 800 mg or ranitidine or nizatidine 300 mg or famotidine 40 mg PO daily at bedtime for 6 weeks

Uncomplicated gastric ulcers:

  • Cimetidine 400 mg or ranitidine or nizatidine 150 mg or famotidine 20 mg PO twice daily for 8 weeks



A) High risk patients related to NSAID induced ulcer requiring prophylactic therapy include:

  • History of ulcers
  • Complicated ulcers
  • Current use of steroids or anticoagulants/antiplatelet agents
  • Age >60 years
  • Serious comorbid illness

Treatment Options:

  • PPIs once daily in doses as mentioned above
  • Change patient to COX-2 selective NSAID (contraindicated in patients with risk of CVD)
  • Misoprostol 200 mcg PO QID

B) Long term maintenance therapy is indicated in patients with recurrent ulcers who are H. pylori negative or have failed attempts of eradication.

Treatment Options:

  • PPIs once daily in doses as mentioned above
  • H2 receptor antagonist at bedtime (cimetidine 400-800 mg or ranitidine or Nizatidine 150-300 mg or famotidine 20-40 mg PO daily)

C) Non-pharmacological therapy includes:

  • Quit smoking
  • Avoid excess alcohol
  • Dietary modification
  • Adequate rest



Perforation presents with (medical emergency)

  • Severe sudden abdominal pain
  • Rigidity
  • Abdominal distension

Treatment options:

  • Simple closure
  • Graham patch with or without a laparoscopic vagotomy (for duodenal ulcers)
  • Truncal vagotomy with pyloroplasty (incorporating the perforation)
  • Preferred approach for gastric ulcers in elderly is partial gastrectomy

Bleeding presents with

  • Hemodynamic instability
  • Hematemesis/hematochezia/melena

- Initial management

  • Resuscitation
  • Medical therapy with intravenous continuous-infusion proton pump inhibitors
  • Rapidly correct coagulopathy with blood products
  • Endoscopic intervention
    • Injection therapy (options):
      • Epinephrine injection
      • Saline injection (to tamponade bleeding vessel)
      • Fibrin sealant or other injection sclerotherapy
    • Note: While various agents have been used to help control bleeding a key feature of injection therapy, regardless of agent, is essentially to tamponade the bleeding vessel. The use of sclerosants may be complicated by perforations and are usually discouraged.
    • Thermal coagulation: May be achieved through direct contact devices (e.g. heater probes, electrocoagulation) and noncontact devices (argon plasma coagulation, APC), which appear to have similar efficacy
    • Endoclips/Hemoclips: May have the distinct advantage of lowering rate of recurrent bleeding as compared to other therapies, but are difficult to apply and so cannot always be utilized
    • Combination therapy: Diluted epinephrine injection followed with thermocoagulation may be a useful approach particularly in high risk patients

- Indications for surgery

  • Hemodynamic instability despite vigorous resuscitation (>3 unit transfusion)
  • Shock associated with recurrent hemorrhage
  • Failure to arrest hemorrhage on endoscopy
  • Recurrent bleeding despite endoscopic attempts at achieving hemostasis

Surgical procedures (brief overview of options)

  • Duodenal ulcers: Inspect and control bleeding; ligate the gastroduodenal artery at the superior and inferior aspect of the ulcer, pyloroplasty possibly combined with truncal vagotomy
  • Gastric ulcers: Resection with Billroth I or II reconstruction may be indicated


  • Penetration through the bowel wall without perforation and leakage of luminal contents into the peritoneal cavity
  • 20% of ulcers penetrate
  • Presents with gradual or sudden change in symptoms
  • Gastrocolic fistulae are seen with greater curvature gastric ulcers


  • Managed with intensive ulcer treatment regimens
  • Surgical options can also be considered

Obstruction presents with

  • Early satiety and bloating
  • Indigestion/epigastric pain
  • Anorexia/weight loss
  • Nausea and vomiting of recognizable food
  • Dehydration/metabolic alkalosis


Gastric outlet obstruction is usually not an emergency

Stabilize patient then consider:

  • Nasogastric tube decompression
  • Correction of fluid and electrolyte
  • Preoperative nutritional supplementation
  • Full dose intravenous antisecretory therapy
  • Endoscopic balloon dilatation
  • Surgical options are:
    • Truncal vagotomy and gastrojejunostomy
    • Antrectomy (rarely performed)
    • Distal gastrectomy, combined with vagotomy


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H2-Receptor Antagonist (H2RA)

  • Cimetidine
  • Ranitidine
  • Famotidine
  • Nizatidine


Inhibits the histamine at H2 receptors of the gastric parietal cells, resulting in decreased secretion of gastric acid.



  • Oral: 400 mg BID or 800 mg once daily
  • strong>IV / IM: 300 mg every 6hrs; Dilute for IV route

Dose in renal insufficiency:

  • Decrease dose by 50% if ClCr 10-50 mL/min
  • Decrease dose by 75% if ClCr <10 mL/min


  • Oral: 150 mg BID or 300 mg once daily
  • IV / IM: 50 mg every 6-8 hrs; dilute for IV route

Dose in renal insufficiency:

  • 150 mg PO daily; if ClCr <50 mL/min


  • Oral: 20 mg BID or 40 mg daily
  • IV: 20 mg every 12 hrs

Dose in renal insufficiency:

  • Decrease dose by 50% if ClCr <50 mL/min


  • Oral: 150 mg BID or 300 mg daily

Dose in renal impairment:

Active treatment:

  • Clcr 20-50 mL/minute: 150 mg/day
  • Clcr <20 mL/minute: 150 mg every other day

Maintenance treatment:

  • Clcr 20-50 mL/minute: 150 mg every other day
  • Clcr <20 mL/minute: 150 mg every 3 days


Proton Pump Inhibitors (PPIs)

  • Omeprazole
  • Lansoprazole
  • Esomeprazole
  • Rabeprazole
  • Pantoprazole


Suppress gastric acid secretion by inhibition of the gastric enzyme H+/K+-ATPase in the gastric parietal cell.



  • 20 mg PO once daily for 4-8 wk.; in refractory patients 40 mg PO daily


  • Duodenal ulcer: 15 mg PO daily for ~4 wk
  • Gastric ulcer: 30 mg PO daily for ~8 wk
  • IV: 30 mg IV daily over 30 min


  • Oral: 20-40 mg daily for 4-8 wk
  • IV: 20-40 mg daily


  • 20 mg PO daily for 4-6 wk


  • 40 mg PO daily for 4-8 wk


Gastroduodenal Cytoprotective Agent-Antacids

  • Sucralfate


Produces an adherent and cytoprotective barrier at the ulcer site by binding with positively charged proteins in exudates, forming a protective coat for ulcer site against peptic acid, pepsin and bile.



Peptic ulcer

  • 1 g PO QID, an hour before meals and at bedtime, on an empty stomach for 4-8 weeks

Duodenal ulcer

  • 2 g PO BID on waking up and at bedtime on an empty stomach for 4-8 weeks

Duodenal ulcer maintenance/prophylaxis

  • 1 g PO BID on an empty stomach


Mucosal Protective Agent

  • Misoprostol


It is a synthetic analog of prostaglandin E1.

  • It replaces the protective prostaglandins that have been depleted due to prostaglandin-inhibiting therapies (e.g. NSAIDs) and also inhibits the acid production
  • It also induces uterine contractions and exhibit a significant cervical priming effect



Duodenal ulcers/Prevention of NSAID-induced ulcers

  • 200 mcg PO QID with food and fourth dose taken at bedtime; if not tolerated, may decrease dose to 100 mcg QID or 200 mcg BID

Note: Administer for the duration of NSAID therapy


H. Pylori Eradication Regimen:

➢ PPI + Amoxicillin + Clarithromycin


➢ PPI + Metronidazole + Clarithromycin


➢ PPI + Amoxicillin + Metronidazole


➢ PPI + Bismuth subsalicylate + Metronidazole +



➢ PPI + Amoxicillin followed by PPI + Clarithromycin +



  • Triple therapy (oral): 2 antibiotics plus a PPI for 14 days
    1. PPI (standard therapy) PO BID PLUS
    2. Amoxicillin 1 g PO BID OR Metronidazole 500 mg PO BID PLUS
    3. Clarithromycin 500 mg PO BID
  • Alternative triple therapy regimen: if clarithromycin resistance is present:
    1. PPI (standard therapy) PO BID PLUS
    2. Amoxicillin 1 g PO BID PLUS
    3. Metronidazole 500 mg PO BID
  • Alternative triple therapy regimen: if penicillin allergic:
    1. PPI (standard therapy) PO BID PLUS
    2. Clarithromycin 500 mg PO BID PLUS
    3. Metronidazole 500 mg PO BID
  • Alternative Quadruple Therapy regimen:
    1. PPI (standard therapy) PO BID PLUS
    2. Bismuth subsalicylate 2 tabs PO QID PLUS
    3. Metronidazole 250 mg PO QID plus
    4. Tetracycline 500 mg PO BID

Sequential therapy

  • PPIs PO BID (as mentioned above) PLUS
  • Day 1-5: Amoxicillin 1 gm PO daily PLUS
  • Day 6-10: Clarithromycin 500 mg and metronidazole 500 mg, both twice daily


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Diagnosis and Goals:


  • Hypovolemia due to hemorrhage
  • Acute epigastric pain, secondary to hypersecretion of acid, mucosal erosion, or perforation
  • Diarrhea related to GI bleeding
  • Imbalanced nutrition due to disease process
  • Deficient knowledge related to physical, dietary, and pharmacologic treatment of disease
  • Acute pain
  • Ineffective therapeutic regimen management
  • Nausea

Potential complication:

  • 3 major complications
    • Hemorrhage
    • Perforation
    • Gastric outlet obstruction
  • Initially treated conservatively
  • May require surgery at any time during course of therapy


Overall Goals

  • Comply with prescribed therapeutic regimen
  • Experience a reduction or absence of discomfort related to peptic ulcer disease
  • Exhibits no signs of GI complications
  • Have complete healing
  • Lifestyle changes to prevent recurrence

Aim of treatment program

  • Decrease the degree of gastric acidity
  • Enhance mucosal defense mechanisms
  • Minimize harmful effects on mucosa
  • Avoid hypovolemia
  • Relieve pain and reduce anxiety
  • Maintain nutrition
  • Ensure there are no complication
  • Provide detailed information about the management and prevention of recurrence
  • Comply with prescribed therapeutic regimen
  • Experience a reduction or absence of discomfort
  • Exhibit no signs of GI complications
  • Have complete healing
  • Lifestyle changes to prevent recurrence


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Nursing Intervention:

Acute exacerbation:

  • Treated with same regimen that is used for conservative therapy
  • Situation is more serious because of possible complications like perforation, hemorrhage, gastric outlet obstruction
  • Accompanied by bleeding, increased pain, discomfort, nausea, and vomiting
  • Recurrent vomiting or gastric outlet obstruction

Acute intervention:

Convey treatment measures to client/family.

Regular mouth and nose care.

Gastric outlet obstruction - Aim is to decompress the stomach, correct fluid and electrolyte imbalances, improve health status.

  • Can occur at any time - likely in clients whose ulcer is located close to pylorus
  • Gradual onset
  • Constant NG aspiration of stomach contents may relieve symptoms
  • Regular irrigation of NG tube
  • Repositioning from side to side
  • IV fluids

Perforation - Immediate focus - Stop spillage of gastric or duodenal contents into peritoneal cavity.

  • Sudden, severe abdominal pain unrelated in intensity and location to pain that brought client to hospital
  • Indicated by a rigid, board like abdomen
  • Severe generalized abdominal and shoulder pain
  • Shallow, grunting respirations
  • Bowel sounds diminished or absent
  • Vital signs every 15 to 30 minutes
  • Stop all oral, NG feeds/drugs until health care provider notified

Avoiding volume deficit:

  • Intake and output charting to determine fluid volume status
  • Monitor vitals hourly, report any change in pulse and BP immediately
  • Monitor stools for blood
  • Check for any blood in vomitus
  • Periodically check hemoglobin, hematocrit and electrolytes
  • Administer IV fluids and blood replacement, as prescribed
  • Insert NG tube as prescribed, and monitor the tube drainage for presence of occult blood
  • Administer medications through the NG tube to neutralize acidity, as prescribed
  • Prepare patient for saline lavage, as ordered
  • Prepare patient for diagnostic procedure or surgery to determine or stop the source of bleeding

Pain relief:

  • Administer medication as prescribed
  • Provide small, frequent meals to prevent gastric distention if not NPO
  • Advise patient about the irritating effects of certain drugs and foods
  • Advise to quit smoking
  • Encourage dietary modification
  • Teach and encourage relaxation techniques

Managing diarrhea:

  • Monitor the pattern to determine the effect of medication on defecation
  • Monitor for signs of dehydration and malnutrition
  • Administer antidiarrheal as prescribed
  • Check for skin integrity around the anus to prevent infections

Achieving Adequate Nutrition:

Dietary modifications may be necessary so that foods and beverages irritating to client can be avoided or eliminated.

  • Provide high-calorie, high-protein diet with nutritional supplements as ordered
  • Diet should consist of:
    • Small, dry feedings daily-6 small meals a day during symptomatic phase
    • Low in carbohydrates
    • Restrict sugar with meals
    • Moderate amounts of protein and fat
    • 30 minutes of rest after each meal
  • In patients with prolonged bleeding or malnutrition, parenteral nutrition is administered as prescribed

Educating the patient about the treatment regimen:

  • Explain all tests and procedures to minimize anxiety
  • Review and verbalize recommendations for diet, activity, medication, and treatment
  • Patient should be provided time for questions, and clarify any misunderstandings
  • Provide written and verbal instructions of medications, dosages, times of administration, and desired effects
  • Teach patient signs and symptoms of bleeding and when to notify the health care provider
  • Provide detailed explanation of all the effects of medications
  • If surgery is planned in future explain what should be expected

Expected outcomes:

  • Vital signs stable; fluid volume maintained
  • Remains free of pain in between meals
  • No more than two to three loose stools per day
  • No weight loss, and is compliant with medications
  • Is well aware of the complications and knows when to go to emergency
  • Have full understanding of his/her disease and is aware of all the side effects of medications


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Nursing Alerts:
  • Sudden, intense epigastric pain radiating to the right shoulder may indicate ulcer perforation
  • Stop antisecretory proton pump inhibitor at least 2 weeks before the C-urea breath test as it can cause false-negative test result


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Core Resources:

  • Compendium of Pharmaceuticals and Specialties (CPS). Canadian Pharmacist association. 2010.Toronto: Webcom.Inc
  • Day RA, Paul P, Williams B et al (2010) Brunner & Suddarth's Textbook of Canadian Medical-Surgical Nursing (2nd ed.)Philadelphia: Lippincot Williams and Wilkins
  • Dirksen, S., Lewis, S., & Collier, I., Heitkemper, M., O'Brien, P., & Bucher, L. (2010). Medical-Surgical Nursing in Canada: Assessment and management of clinical problems (2nd ed.). Toronto: Mosby Elsevier.
  • Foster C, Mistry NF, Peddi PF, Sharma S ; (2010) The Washington Manual of Medical Therapeutics (33rd ed) Philadelphia:Lippincot Williams and Wilkins
  • Gray J, (2007) Therapeutic Choices. Canadian Pharmacists Association (5th ed)Toronto: Webcom.Inc
  • Holbrook AM (Chair) for Ontario GI Therapy Review Panel. Ontario Guidelines for Peptic Ulcer Disease and Gastroesophageal Reflux. Toronto. First Edition. Queen's Printer of Ontario, 2000.
  • Hurst's the Heart Manual of Cardiology, 12th Edition
  • Katzung BG, Masters SB, Trevor AJ (2009) Basic and clinical Pharmacology (11th ed) McGraw Hill
  • Longo D, Fauci A, Kasper D et al. 2011Harrison's Principles of Internal Medicine,(18th ed)
  • McPhee SJ, Papadakis MA (2010) Current Medical Diagnosis & Treatment (49th ed) New York, McGraw Hill
  • Pagana KD, Pagana TJ eds. Mosby's Diagnostic and Laboratory Test Reference. 9th ed. St. Louis: Elsevier-Mosby; 2009
  • Skidmore-Roth L. ed. Mosby's drug guide for nurses. 9th ed. St. Louis: Elsevier-Mosby; 2011
  • Skidmore-Roth L, ed. Mosby's nursing drug reference. 24 th ed. St. Louis: Elsevier-Mosby; 2011

Online Pharmacological Resources:

  • e-Therapeutics
  • Lexicomp
  • RxList
  • Epocrates

Journals/Clinical Trials:

  • Bhatt DL, Cryer BL, Constant CF, et al. Clopidogrel with or without Omeprazole in Coronary Artery Disease N Engl J Med 2010; 363:1909-1917
  • Chan FKL, To KF, Wu JCY et al. outline goes here Eradication of Helicobacter pylori and risk of peptic ulcers in patients starting long-term treatment with non-steroidal anti-inflammatory drugs: a randomized trial.The Lancet, 2002 ;(359), pgs.9-13.
  • Khuroo MS, Yattoo GN, Javid G et al. A comparison of omeprazole and placebo for bleeding peptic ulcer. N Engl J Med. 1997;336(15):1054-8
  • Kubba AK, Palmer KR. Role of endoscopic injection therapy in the treatment of bleeding peptic ulcer. Br J Surg 1996; 83:461.
  • Lai KC, Hui WM, Wong BC, et al. A retrospective and prospective study on the safety of discharging selected patients with duodenal ulcer bleeding on the same day as endoscopy. Gastrointest Endosc. 1997; 45:26
  • Lau J.Y.W., Sung J.J.Y., Lee K.K.C., et al. Effect of Intravenous Omeprazole on Recurrent Bleeding after Endoscopic Treatment of Bleeding Peptic Ulcers N Engl J Med 2000; 343:310 - 316
  • Marshall BJ, Warren JR et al. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet. 1984;1(8390):1311-5.
  • Park CH, Joo YE, Kim HS, et al. A prospective, randomized trial comparing mechanical methods of hemostasis plus epinephrine injection to epinephrine injection alone for bleeding peptic ulcer. Gastrointest Endosc 2004; 60:173.
  • Vaira D, Zullo A, Vakil N et al. Sequential therapy versus standard triple drug therapy for H.pylori eradication: a randomized trial. Ann Intern Med. 2007;146(8):556-63


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Samir C. Grover, MD, MEd, FRCPC, Consultant, Division of Gastroenterology, St. Michael's Hospital, Assistant Professor, Department of Medicine, University of Toronto, ON Canada
.......................................... NURSING EDITOR:
Sadie Sattan, RN, BScN, MN School of Nursing, Faculty of Health Sciences McMaster University/Mohawk College Hamilton, ON Canada

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