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Description : Check out this medical presentation on Peptic Ulcer Disease, which is titled "Gastroenterology: Peptic Ulcer Disease", to know about the common forms of peptic ulcer disease (PUD).

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Published on : Jul 10, 2021 | Views : 1862 | Downloads : 14

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Slide 1-

Gastroenterology: Peptic Ulcer Disease Courses in Therapeutics and Disease State Management
Slide 2-

Learning Objectives (Slide 1 of 2) Identify and compare the common forms of peptic ulcer disease (PUD). Describe features associated with Helicobactor pylori-associated and NSAID-induced ulcers. Discuss the role of Helicobacter pylori (HP) in PUD. Compare and contrast signs and symptoms of duodenal and gastric ulcers. Identify, describe, and discuss the utility of laboratory tests used to detect the presence of HP
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Learning Objectives (Slide 2 of 2) Discuss pharmacologic treatment options for HP-associated and NSAID-induced PUD. Given a PUD patient history, recommend appropriate pharmacologic therapy and explain the rationale behind your decision Discuss drug adverse effects and monitoring parameters for drugs and disease states Construct counseling points for a PUD patient on their disease state and pharmacologic therapy
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Required Reading Love BL, Mohorn PL. Peptic Ulcer Disease and Related Disorders. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L. eds. Pharmacotherapy: A Pathophysiologic Approach, 10e New York, NY: McGraw-Hill; 2017.
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Overview Peptic ulcer disease (PUD) refers to ulceration of the mucosa anywhere in the GI tract exposed to acid and pepsin They can range in size from a few millimeters to a few centimeters Estimated that 10% of Americans will develop PUD in their lifetime The 2 most common forms/locations of PUD are Duodenal ulcer Gastric ulcer
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Duodenal Ulcers Most common form of PUD It is 3 times more common than gastric ulcers Usually located in the duodenal bulb of the small intestine Most commonly occurs in people between the ages of 30 and 50
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Gastric Ulcers Less common than duodenal ulcers Especially in the absence of chronic NSAID use Most commonly located in the lesser curvature of the antrum of the stomach More common in people greater than 60 years old
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Anatomical View of Duodenal and Gastric Ulcers Link: Anatomic structure of the stomach and duodenum and most common locations of gastric and duodenal ulcers.
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Photos of Duodenal and Gastric Ulcers Link: Figure of a Duodenal Ulcer Link: Figure of a Duodenal Ulcer and a Gastric Ulcer
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Etiology and Pathophysiology (Slide 1 of 2) Gastric and duodenal ulcers develop because of an imbalance between aggressive factors and mechanisms that maintain mucosal integrity There is an increase in mucosal injury and a decrease in mucosal defense Aggressive factors (H. pylori, NSAIDs) cause mucosal injury and a decrease in mucosal defenses and healing (decreased mucous, decreased bicarbonate, decreased mucosal blood flow)
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Etiology and Pathophysiology (Slide 2 of 2) Common causes of PUD Helicobacter pylori (H.pylori) infection Nonsteroidal Anti-inflammatory Drugs (NSAIDs) Critical illness (stress-related mucosal damage) Uncommon causes of PUD Idiopathic (non-H.pylori, non- NSAID) Hypersecretion of gastric acid (e.g. Zollinger Ellison syndrome) Viral infections Radiation therapy Chemotherapy
Slide 12-

Helicobacter Pylori (HP)-Associated (Slide 1 of 4) Helicobacter pylori (HP) is a spiral shaped, gram negative, flagellated bacteria first associated with PUD in the early 1980’s Found in most people with duodenal and gastric ulcers About 95% of those with duodenal ulcers About 80% of those with gastric ulcers
Slide 13-

Helicobacter Pylori (HP)-Associated (Slide 2 of 4) Approximately 30% - 40% of the U.S. population is infected About 15% of those infected will develop PUD HP is primarily spread through the fecal to oral route People are most often infected during childhood
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Helicobacter Pylori (HP)-Associated (Slide 3 of 4) Mechanisms by which HP causes mucosal injury are not entirely clear but occurs through a combination of the following mechanisms: HP catalyzes urea  ammonia is produced  ammonia erodes the mucous barrier and causes epithelial damage HP produces cytotoxins HP produces mucolytic enzymes
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Helicobacter pylori (HP)-Associated (Slide 4 of 4) Link: Schematic of the relationships between colonization with Helicobacter pylori and diseases of the upper gastrointestinal tract
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NSAID-Induced (Slide 1 of 4) In long-term NSAID users, there is a 10% - 20% prevalence of gastric ulcers and a 2% - 5% prevalence of duodenal ulcers Mechanisms for NSAID-induced ulceration NSAIDs are weak acids and are non-ionized at gastric pH Diffuse freely across the mucous barrier into gastric epithelial cells  H+ ions are liberated and cause cellular damage
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NSAID-Induced (Slide 2 of 4) Mechanisms for NSAID-induced ulceration (continued) NSAIDs inhibit cyclooxygenase activity and therefore decrease prostaglandin production which results in a: Reduction in gastric and mucosal blood flow Decrease in mucous and bicarbonate secretion Decrease in cellular repair and replication Link: Figure showing mechanisms by which nonsteroidal anti-inflammatory drugs may induce mucosal injury
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NSAID-Induced (Slide 3 of 4) 1% - 2% of NSAID users will develop an ulcer or ulcer complications with 1 year The risk of developing an NSAID-related complication is greater in patients: Greater than 60 years old With a prior history of PUD Taking high dose NSAIDs or multiple NSAIDs, including low dose aspirin
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NSAID-Induced (Slide 4 of 4) The risk of developing an NSAID-related complication is greater in patients (continued): Who are concurrently taking Corticosteroids Anticoagulants Oral bisphosphonates Anti-platelet agents SSRIs (Selective Serotonin Reuptake Inhibitors) Aspirin is the most ulcernogenic of all NSAIDs. Even with low dose aspirin (81-162mg/day), ulcers occur in 0.6% - 1.2% of patients per year.
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Zollinger-Ellison Syndrome (ZES) ZES is characterized by gastric acid hypersecretion and recurrent peptic ulcers that result from a gastrin-producing tumor More than 50% of gastrinomas are malignant ZES is suspected for patients with multiple ulcers and recurrent or refractory PUD often accompanied by esophagitis or ulcer complications Only accounts for 0.1% to 1% of those with duodenal ulcer
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Other Potential Factors in the Development of PUD Cigarette smoking Increases the risk of developing PUD and its complications Impairs ulcer healing and increases the risk of recurrence Ulcer risk is proportional to the number of cigarettes smoked per day Psychological stress People who develop PUD tend to be more adversely affected by stress However, controlled trials are conflicting and have failed to document a direct cause-effect relationship Stress may induce behavioral risks such as smoking and the use of NSAIDs or may alter the inflammatory response or resistance to HP infection Dietary factors Certain foods (e.g. coffee, tea, carbonated beverages, beer, milk, spices) may cause dyspepsia but do not increase the risk of developing PUD
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Signs and Symptoms (Slide 1 of 3) Symptoms depend on ulcer location, ulcer etiology, and patient age Many patients, particularly the elderly, have few or even no symptoms NSAID-induced ulcers are often silent Complications such as bleeding and perforation are often the initial presentation
Slide 23-

Signs and Symptoms (Slide 2 of 3) Pain localized to the epigastrium is the most common symptom The pain is described as burning, gnawing, cramping, or hunger A typical nocturnal pain that wakes the patient from sleep (especially between 12 and 3am) The severity of ulcer pain varies from patient to patient and my be seasonal, occurring more often in the spring or fall
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Signs and Symptoms (Slide 3 of 3) Episodes of pain usually occur in clusters, lasting up to a few weeks followed by a pain-free period or remission lasting weeks to years Changes in the character of pain may suggest the presence of complications Pyrosis (heartburn), belching, and bloating may accompany the pain
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Gastric Ulcer Pain often does not follow a consistent pattern; not predictable Food will sometimes cause or accentuate pain Nausea, vomiting, anorexia, and weight loss are more common with gastric ulcer than duodenal ulcer
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Duodenal Ulcer Pain more likely follows a consistent pattern (compared to gastric ulcer) Epigastric pain occurs in 60% - 90% of patients with duodenal ulcers Food often relieves pain but the pain usually returns 1 to 3 hours after eating Nocturnal epigastric pain often occurs 40% - 70% have additional non-specific dyspeptic complaints (belching, bloating, abdominal distension, food intolerance)
Slide 27-

Clinical Presentation Link: Table on Comparison of Common Forms of Peptic Ulcer Link: Table on Clinical Presentation of Peptic Ulcer Disease
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Complications Major complications of PUD include: Bleeding Occurs in about 15% of patients with active PUD Perforation Occurs in about 7% of patients with active PUD Mortality Mortality from acute bleeding is about 6% - 10%
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Bleeding and Hemorrhage in Peptic Ulcers Link: Figure of stigmata of hemorrhage in peptic ulcers
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Role of Testing The diagnosis of PUD depends on visualizing the ulcer crater by either upper GI radiography or upper endoscopy Upper GI radiography with barium was the initial diagnostic procedure but has been replaced with upper endoscopy There are multiple laboratory tests that can be performed to diagnosis an H.pylori infection
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Testing for H. pylori There are multiple tests that can be performed to test for the presence of H. pylori Invasive testing (Requires endoscopy with biopsy) Histology Culture Rapid urease testing Noninvasive testing Serological test Urea breath test Fecal antigen test
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Invasive Testing (Slide 1 of 2) All of these tests require biopsy to be acquired via endoscopy Histology Microbiologic examination using various stains Excellent sensitivity and specificity but it is invasive, expensive and requires trained personnel Culture Culture of biopsy Costly, time consuming, and technically difficult
Slide 33-

Invasive Testing (Slide 2 of 2) Rapid Urease Testing Rapid urease tests detect the presence of ammonia in the biopsy sample The ammonia is generated by H.pylori urease activity Test of choice at endoscopy Greater than 90% sensitive and specific Easily performed with rapid results Tests for active HP infection
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Noninvasive Tests (Antibody Detection/Serological Test) A simple blood test Laboratory-based (more accurate than office-based tests) Office-based Detects IgG antibodies to H. pylori in the serum Quick, noninvasive, inexpensive but has a low positive predictive value in populations where prevalence of HP infection is low. Can’t be used to distinguish between an active infection or past exposure because antibodies persist for long periods of time Most patients remain seropositive for 6 months to 1 year after HP eradication Can’t be used to determine if eradication is successful
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Noninvasive Tests (Urea Breath Test) Detects the exhalation of radioactive CO2 following ingestion of 13C or 14C radiolabeled urea H. pylori hydrolysis of the radiolabeled urea results in radiolabeled CO2 production 97% sensitivity and 95% specificity
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Noninvasive Tests (Fecal Antigen Test) Polyclonal antibody test that detects the presence of H.pylori antigen in the stool Sensitivity and specificity similar to urea breath test Patients may have a reluctance to collect stool samples
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Noninvasive Tests (Notes) The urea breath and fecal antigen tests may be falsely negative in patients who have recently taken Antibiotics (up to 4 weeks) Bismuth compounds (up to 4 weeks) Antisecretory agents (up to 2 weeks) The urea breath and fecal antigen tests can be used as an initial screen to determine if a patient is infected
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Tests for Confirming Eradication The urea breath (preferred) and fecal antigen tests can be used to confirm eradiation of H.pylori in a patient who has been treated The serological test can not be used to determine eradication because antibodies last for an extended period after the infection has been cleared However, confirming eradication is not practical or cost effective Indications for confirming eradication include: Continued dyspeptic symptoms H. pylori-associated MALT (mucosal associated lymphoid tissue) lymphoma Resection for gastric cancer
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Testing for H. pylori Link: Table covering tests for the detection of Helicobacter pylori
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Treatment/Therapy Goals Choice of treatment depends on etiology (e.g. HP or NSAIDs) and whether treatment is for initial management or prevention of recurrence Overall goals Relief of pain Healing of ulcer Prevention of recurrence Prevent or reduce complications
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Nonpharmacologic Therapy Eliminate or reduce psychological stress Smoking cessation Eliminate or reduce NSAID use Avoid foods that cause dyspepsia
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Pharmacologic Therapy Overview For an active HP positive ulcer, our goals are to eradicate the HP, heal the ulcer, and ultimately cure the disease Use multi-drug regimens containing antibiotics and anti-secretory agents (usually proton pump inhibitors (PPIs)) and sometimes bismuth preparations For an NSAID-induced peptic ulcer or a peptic ulcer is not caused by HP, our primary goal is to heal the ulcer as quickly as possible Can use PPIs, H2-receptor antagonists, or sucralfate Antacids are not used as monotherapy to heal peptic ulcers Misoprostol can be used to reduce the risk of NSAID-induced PUD
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Proton Pump Inhibitors (PPIs) (Slide 1 of 3) MOA Blocks acid secretion by inhibiting gastric H+/K+ adenosine triphosphatase found on the secretory surface of gastric parietal cells Results in a long-lasting anti-secretory effect that can maintain gastric pH levels above 4 Agents Dexlansoprazole (Dexilant) Esomeprazole (Nexium) Lansoprazole (Prevacid) Omeprazole (Prilosec) Omeprazole/sodium bicarbonate (Zegerid) Pantoprazole (Protonix) Rabeprazole (Aciphex)
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Proton Pump Inhibitors (PPIs) (Slide 2 of 3) Common adverse effects Headache, dizziness, somnolence, diarrhea, constipation, flatulence, abdominal pain, nausea Serious adverse effects Increased risk of Clostridium difficile infections Increase risk of community-acquired pneumonia Long-term adverse effects (> 1 year) Hypomagnesemia Bone fractures Vitamin B12 deficiency
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Proton Pump Inhibitors (PPIs) (Slide 3 of 3) Monitoring Appearance of diarrhea (frequency and type of diarrhea episodes) Periodic magnesium levels (if long-term therapy) Routine bone density studies (DXA scans) If other risk factors for osteoporosis or bone fractures present Patient counseling Preferable to take a PPI 30 to 60 minutes before a meal (mainly breakfast) If a second dose is needed, take prior to the evening meal Onset of relief is 2 to 3 hours and the duration of relief is 12 to 24 hours
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Evaluate the Risks versus Benefits of Long-Term PPI Use (Slide 1 of 2) Long-term PPI use has been associated with increased risk of: Fractures Infections such as C. Diff and pneumonia (expand) Hypomagnesemia Vitamin B12 deficiency
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Evaluate the Risks versus Benefits of Long-Term PPI Use (Slide 2 of 2) Long-term PPI use MAY BE associated with increased risk of: Dementia Renal disease Cardiovascular disease
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H2-Receptor Antagonists (Slide 1 of 2) MOA Competitive inhibition of histamine at H2 receptors of gastric parietal cells which inhibits gastric acid secretion Agents Cimetidine (Tagamet) Famotidine (Pepcid) Nizatidine (Axid) Ranitidine (Zantac)
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H2-Receptor Antagonists (Slide 2 of 2) Adverse effects Headache, somnolence, fatigue, dizziness, constipation, diarrhea Monitoring Monitor for CNS effects (rare) in those over 50 years old or in those with renal or hepatic impairment Patient counseling If taking once a day, it is preferable to take the dose at bedtime Onset of relief is 30 to 45 minutes and duration of relief is 4 to 10 hours
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Misoprostol (Slide 1 of 2) MOA A synthetic prostaglandin E1 analog that replaces the protective prostaglandins that are decreased from prostaglandin inhibiting therapies such as NSAIDs Enhances natural gastromucosal defense mechanisms and healing by increasing the production of gastric mucous and mucosal secretion of bicarbonate Inhibits basal and nocturnal acid secretion by direct action on the parietal cells Agent Misoprostol (Cytotec) Adverse effects Diarrhea, abdominal pain, headache, nausea/vomiting, flatulence, dysmenorrhea, hypophosphatemia
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Misoprostol (Slide 2 of 2) Monitoring Pregnancy test Serum phosphate Patient Counseling Pregnancy category X Is a potential abortifacient
Slide 52-

Bismuth Preparations (Slide 1 of 2) MOA Bismuth exhibits antimicrobial activity against bacterial and viral gastrointestinal pathogens Agents Bismuth subsalicylate (Pepto-Bismol and others) Bismuth subcitrate potassium (bismuth salt in Pylera capsules) Adverse effects Fecal discoloration, tongue discoloration Neurotoxicity (rare)
Slide 53-

Bismuth Preparations (Slide 2 of 2) Monitoring No specific monitoring Patient counseling May cause temporary, harmless darkening of the tongue and/or stool Avoid bismuth subsalicylate if have an aspirin allergy
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Sucralfate (Slide 1 of 2) MOA Thought to form an ulcer-adherent complex at the ulcer site protecting it from further injury from stomach acid Agent Sucralfate (Carafate) Adverse Effects Constipation, bezoar formation, hyperglycemia in diabetes patients, aluminum toxicity in patients with chronic renal failure or on dialysis
Slide 55-

Sucralfate (Slide 2 of 2) Monitoring Blood glucose in diabetes patients Renal function in elderly patients Patient counseling Take on an empty stomach Do not take antacids 30 minutes before or after taking sucralfate
Slide 56-

Antacids (Slide 1 of 2) MOA Neutralize hydrochloric acid in the stomach, which results in an increase in gastric pH Agents Magnesium hydroxide Aluminum hydroxide Calcium carbonate Adverse effects Diarrhea (magnesium hydroxide) Constipation (aluminum hydroxide and calcium carbonate) Alterations in mineral metabolism Acid-base disturbances
Slide 57-

Antacids (Slide 2 of 2) Monitoring Periodic calcium and phosphate levels if on chronic antacid therapy Patient counseling Antacids can decrease the levels of numerous other drugs including tetracyclines, digoxin, iron supplements, fluroquinolones, and ketoconazole. Patients should separate antacids and other medications by at least 2 hours Patients with renal impairment should not use aluminum or magnesium containing antacids unless directed by their physician Onset of relief is less than 5 minutes and duration of relief is 20 to 30 minutes Link: Table on Composition and Acid Neutralizing Capacities of Popular Antacid Preparations
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Drug Used in PUD Therapy Regimens Link: Drug Dosing Table Link: Drug Monitoring Table
Slide 59-

Treatment of H. pylori-Positive Ulcers Multi-drug regimens that include antimicrobials and anti-secretory agents are used to eradicate H. pylori infection H. pylori has been developing resistance to some antibiotics, particularly clarithromycin First-line therapies should have an eradication rate of greater than 80% Regional bacterial resistance patterns need to be taken into account when recommending therapy If a second course of H. pylori eradication therapy is needed, the second regimen should contain different antibiotics H.pylori eradication regimens Triple Therapy Bismuth-based Quadruple Therapy Sequential Therapy Salvage Therapy
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Triple Therapy (Slide 1 of 2) Standard triple therapy regimen contains Amoxicillin 1000mg twice day PLUS Clarithromycin 500mg twice a day PLUS a PPI dosed once to twice a day Given for 10 to 14 days 14 day regimens are generally preferred as 14 day regimens significantly increases the eradication rate If the patient is allergic to penicillin, then metronidazole 500mg twice a day can be substituted for the amoxicillin
Slide 61-

Triple Therapy (Slide 2 of 2) Standard triple therapy is considered first-line in areas where the clarithromycin resistance rate of H. pylori is less than 20% Adding probiotics (specifically Saccharomyces boulardii and Lactobacillus) to triple therapy has been shown to increase eradication rates and decrease adverse effects of treatment, particularly diarrhea
Slide 62-

Bismuth-based Quadruple Therapy (Slide 1 of 2) Bismuth-based quadruple-therapy contains Tetracycline 500mg 4 times day PLUS Metronidazole 250-500mg 4 times a day PLUS Bismuth subsalicylate 525mg 4 times a day PLUS a PPI once or twice a day OR H2-receptor antagonist twice a day Pylera is a brand name product that is a 3 in 1 capsule Each capsule contains Tetracycline 125mg, Metronidazole 125mg, and Bismuth subcitrate potassium 140mg Dose is 3 capsules 4 times a day plus a PPI twice a day Bismuth-based quadruple regimens are given for 10 to 14 days
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Bismuth-based Quadruple Therapy (Slide 2 of 2) May be used as first-line therapy in areas where the clarithromycin resistance rate is ≥ 20% May also be considered for first-line therapy in those with penicillin allergy or in those who have been previously treated with a macrolide antibiotic May also be used if first-line standard triple therapy fails (e.g. as second-line therapy or salvage therapy)
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Sequential Therapy (Slide 1 of 2) Newer HP eradication therapy where the antibiotics are administered in a sequence rather than at the same time Sequential therapy contains: A PPI twice a day for 10 days AND Amoxicillin 1000mg twice day days 1 – 5, followed by Clarithromycin 500mg twice day PLUS Tinidazole 500mg OR Metronidazole 500mg twice a day days 6 – 10. Given for 10 days total (5 days for each antibiotic regimen)
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Sequential Therapy (Slide 2 of 2) Adherence and tolerance rates of sequential therapy are similar to triple therapy but the cost is lower The American College of Gastroenterology (ACG) Guidelines state that additional validation of sequential therapy needs to occur in North America before it is recommended as a first-line regimen
Slide 66-

Levofloxacin-Based Triple Therapy Levofloxacin-based Triple Therapy contains: Amoxicillin 1000mg twice a day PLUS Levofloxacin 500mg once a day PLUS a PPI twice a day Given for 10 days This regimen is an option for salvage therapy in patients who have persistent H. pylori infection This therapy regimen needs validation in North America
Slide 67-

PPI after H. pylori Eradication Therapy Completion When treating an active ulcer, anti-secretory therapy with a PPI is usually continued for 2 weeks after completing the eradication therapy regimen Typically PPI treatment beyond 2 weeks after completion of eradication therapy is not needed for ulcer healing
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Treatment of NSAID-Induced Ulcers (Slide 1 of 2) Ideally, discontinue the NSAID and treat with standard healing regimens of a PPI, H2-receptor antagonist, or sucralfate Link: Drug Dosing Table PPIs are usually preferred because they provide the fastest symptom relief and ulcer healing
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Treatment of NSAID-Induced Ulcers (Slide 2 of 2) If the NSAID needs to be continued: Consider: Reducing the dose of the NSAID OR Change NSAID to one of the following Acetaminophen A nonacetylated salicylate (salsalate, trisalicylate) A partially selective COX-2 inhibitor (etodalac, nabumetone, meloxicam, diclofenac, celecoxib) Use a PPI to treat the ulcer When an NSAID needs to be continued, PPIs are the drugs of choice to treat and heal the ulcer
Slide 70-

Reducing the Risk of NSAID-Induced Ulcer and GI Complications Strategies to reduce the risk of NSAID-induced ulcers In GI toxicity high risk patients, use either a PPI or misoprostol as co-therapy along with the NSAID Use a selective COX-2 inhibitor instead of a nonselective NSAID When selecting a strategy, cardiovascular risk of the patient must also be considered
Slide 71-

GI and Cardiovascular Safety Issues with NSAIDs (Slide 1 of 2) There is no difference in cardiovascular risk between the selective COX-2 inhibitors, the partially selective NSAIDs, and the non-selective NSAIDs with the exception of naproxen When compared with all the other NSAIDs, naproxen has the best cardiovascular safety profile Link: Table on Risk Factors Associated with NSAID-Induced Ulcers and Upper GI Complications
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GI and Cardiovascular Safety Issues with NSAIDs (Slide 2 of 2) Guidelines for reducing GI risk for patients receiving chronic NSAID therapy Link: Table on Guidelines for Reducing GI Risk for Patients Receiving Chronic NSAID Therapy Guidelines take both CV risk and GI toxicity risk into account when recommending a strategy to reduce the risk of developing a peptic ulcer in those who need chronic NSAID therapy
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Treatment of Non-H. pylori, Non-NSAID Ulcers Very few patients have non-H. pylori, non-NSAID (idiopathic) peptic ulcers If an idiopathic peptic ulcer is confirmed, treatment with standard ulcer healing therapy should be initiated Standard H2-receptor antagonist or sucralfate dosage regimens heal the majority of gastric and duodenal ulcers in 6 to 8 weeks Standard PPI dosage regimens heal the majority of gastric and duodenal ulcers in 4 weeks Link: Drug Dosing Table
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Maintenance Therapy with Anti-Secretory Agents Maintenance therapy (to maintain ulcer healing, prevent recurrence and complications) with anti-secretory agents like PPIs is only indicated in the following groups of high risk patients: Those who have failed H. pylori eradication Those who have a history of ulcer related complications Those who have frequent recurrences of H. pylori-negative ulcers Those who are heavy smokers Those who NSAID users Standard maintenance doses as listed in Drug Dosing Table are appropriate for most of these patients
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Treatment of Gastric Acid Hypersecretion from Zollinger-Ellison Syndrome (ZES) PPIs are the oral drugs of choice for managing gastric acid hypersecretion from ZES Treatment should be started with omeprazole 60mg per day or an equivalent dose of another PPI This PPI daily dose should be divided and the PPI given every 8 to 12 hours Additional pharmacologic and non-pharmacologic treatments are instituted depending on the gastrinoma itself and any other complications that may be present
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Treatment of Refractory Ulcers Ulcers are considered refractory to therapy when symptoms, ulcers, or both persist beyond 8 to 12 weeks despite conventional treatment as previously described or when several courses of H. pylori eradication therapy fail Patient should undergo an upper endoscopy to assess the situation Treatment depends on cause and may include additional H. pylori eradication attempts, higher PPI dosages, or surgery
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Evaluation and Management of PUD Link: Algorithm for the evaluation and management of PUD
Slide 78-

Additional Patient Counseling Discuss with the patient the cause of the ulcer (e.g. H. pylori, NSAIDs, etc.) Address risk factors (e.g. NSAID use, cigarette smoking, etc.) Discuss the rationale behind the multi-drug regimens and the importance of adherence and sticking to the full course of therapy Caution patient to look out for signs of GI bleeding (e.g. tarry stools, abdominal pain, vomiting with evidence of blood)
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References (Slide 1 of 4) Atherton JC, Blaser MJ. Helicobacter pylori Infections. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 19e. New York, NY; McGraw-Hill; 2015. Kee Song L, Topazian M. Gastrointestinal Endoscopy. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 19e. New York, NY: McGraw-Hill; 2015. Del Valle J. Peptic Ulcer Disease and Related Disorders. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 19e. New York, NY: McGraw-Hill; 2015.
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References (Slide 2 of 4) Love BL, Thoma MN. Chapter 20. Peptic Ulcer Disease. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L. eds. Pharmacotherapy: A Pathophysiologic Approach, 9e. New York, NY: McGraw-Hill; 2014. Wallace JL, Sharkey KA. Pharmacotherapy of Gastric Acidity, Peptic Ulcers, and Gastroesophageal Reflux Disease. In: Brunton LL, Chabner BA, Knollmann BC. eds. Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 12e. New York, NY: McGraw-Hill; 2011. Martin CP, Talbert RL. Section 5. Gastroenterology. In: Martin CP, Talbert RL. eds. Pharmacotherapy Bedside Guide. New York, NY: McGraw-Hill; 2013.
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References (Slide 3 of 4) Chey WD, Wong B, et al. American College of Gastroenterology Guideline on the Management of Helicobacter pylori Infection. Am J Gastroenterol 2007; 102: 1808-1825. Graham DY, Fischbach L. Helicobacter pylori treatment in the era of increasing antibiotic resistance. Gut 2010; 59: 1143-1153. Rimbara E, Rischbach LA, Graham DY. Optimal therapy for Helicobacter pylori infections. Nat Rev Gastroenterol Hepatol 2011; 8: 78-88. Chuah SK, Tsay FW, Hsu PI, Wu DC. A new look at anti-Helicobacter pylori therapy. World J Gastroenterol 2011; 17: 3971-3975.
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References (Slide 4 of 4) Micromedex Solutions. Truven Health Analytics, Inc. Ann Arbor, MI. Accessed November 1, 2016. Lexicomp Online®, Lexi-Drugs®, Hudson, Ohio: Lexi-Comp, Inc. Accessed November 1, 2016.