Gastroenterology - 02 (1) - Peptic Ulcer Disease (Courses in Therapeutics and Disease State Management)

Gastroenterology:
Peptic Ulcer Disease

Courses in Therapeutics and Disease State Management
Author: Monica L. Skomo, B.S., Pharm.D., BCACP, CTTS; Assoc. Prof. of Pharmacy Practice; Dir. of Assessment and Educational Strategies; Duquesne University School of Pharmacy
http://accesspharmacy.mhmedical.com/LearningModuleGroup.aspx?id=8
Copyright © 2017 McGraw-Hill Education. All rights reserved
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
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
Required Reading
Love BL, Mohorn PL. Peptic Ulcer Disease and Related Disorder
s. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Pose
y L. eds.
Pharmacotherapy: A Pathophysiologic Approach, 10e
New York, NY: McGraw-Hill; 2017.
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
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
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
Anatomical View of Duodenal and Gastric Ulcers
Link:
Anatomic structure of the stomach and duodenum and most com
mon locations of gastric and duodenal ulcers.
Photos of Duodenal and Gastric Ulcers
• Link: Figure of a Duodenal Ulcer
• Link: Figure of a Duodenal Ulcer and a Gastric Ulcer
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)
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
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 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
(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
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
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
• 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-inflam
matory drugs may induce mucosal injury
• 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
• 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.
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
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
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
• 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
• 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
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
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)
Clinical Presentation
• Link: Table on Comparison of Common Forms of Peptic Ulcer
• Link: Table on Clinical Presentation of Peptic Ulcer Disease
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%
Bleeding and Hemorrhage in Peptic Ulcers
Link: Figure of stigmata of hemorrhage in peptic ulcers
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
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
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
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
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
Noninvasive Tests (Urea Breath Test)
• Detects the exhalation of radioactive CO 2 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
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
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
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
Testing for H. pylori
Link: Table covering tests for the detection of

Helicobacter pylori
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
Nonpharmacologic Therapy
• Eliminate or reduce psychological stress
• Smoking cessation
• Eliminate or reduce NSAID use
• Avoid foods that cause dyspepsia
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
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)
• 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
• 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
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
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
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)
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
– 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
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
Misoprostol (Slide 2 of 2)
• Monitoring
– Pregnancy test
– Serum phosphate
• Patient Counseling
– Pregnancy category X
• Is a potential abortifacient
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)
Bismuth Preparations (Slide 2 of 2)
• Monitoring
– No specific monitoring
– May cause temporary, harmless darkening of the tongue and/or stool
– Avoid bismuth subsalicylate if have an aspirin allergy
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
Sucralfate (Slide 2 of 2)
• Monitoring
– Blood glucose in diabetes patients
– Renal function in elderly patients
– Take on an empty stomach
– Do not take antacids 30 minutes before or after taking sucralfate
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
Antacids (Slide 2 of 2)
• Monitoring
– Periodic calcium and phosphate levels if on chronic antacid therapy
– 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
Drug Used in PUD Therapy Regimens
• Link: Drug Dosing Table
• Link: Drug Monitoring Table
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
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
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
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
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)
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)
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
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
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
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
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
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
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
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
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
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
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
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
Evaluation and Management of PUD
Link: Algorithm for the evaluation and

management of PUD
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)
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.
• 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.
• 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.
• 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.

Gastroenterology - 02 (1) - Peptic Ulcer Disease (Courses in Therapeutics and Disease State Management)

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Gastroenterology - 02 (1) - Peptic Ulcer Disease (Courses in Therapeutics and Disease State Management)

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Gastroenterology:

Peptic Ulcer Disease

• Link: Figure of a Duodenal Ulcer

• Link: Figure of a Duodenal Ulcer and a Gastric Ulcer

Link: Schematic of the relationships between colonization with

• Link: Table on Comparison of Common Forms of Peptic Ulcer

• Link: Table on Clinical Presentation of Peptic Ulcer Disease

Link: Figure of stigmata of hemorrhage in peptic ulcers

Link: Table covering tests for the detection of

• Link: Drug Dosing Table

• Link: Drug Monitoring Table

Link: Algorithm for the evaluation and

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