Transcript Chapter_078
Chapter 78
Drugs for Peptic Ulcer Disease
Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc.
Peptic Ulcer Disease
Definition
Group of upper GI disorders
Degrees of erosion of the gut wall
Severe erosion can be complicated by
hemorrhage and perforation
Cause
Imbalance between mucosal and aggressive
factors
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Fig. 78–1. The relationship of mucosal defenses and aggressive factors to health and peptic ulcer
disease. When aggressive factors outweigh mucosal defenses, gastritis and peptic ulcers result.
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Pathogenesis of Peptic Ulcers
Defensive factors
Mucus
• Secreted cells of the GI mucosa
• Forms a barrier to protect underlying cells from acid and pepsin
Bicarbonate
• Secreted by epithelial cells of stomach and duodenum
• Most remains trapped in the mucus layer to neutralize
hydrogen ions that penetrate the mucus
Blood flow
• Poor blood flow can lead to ischemia, cell injury, and
vulnerability to attack
Prostaglandins
• Stimulate the secretion of mucus and bicarbonate
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Pathogenesis of Peptic Ulcers
Aggressive factors
Helicobacter pylori, also known as H. pylori
• Gram-negative bacillus that can colonize in the stomach
and duodenum
• Lives between epithelial cells and the mucus barrier
Escapes destruction by acid
• Can remain in GI tract for decades
• Half of the world infected, but most people do not
develop symptomatic peptic ulcer disease (PUD)
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Pathogenesis of Peptic Ulcers
Aggressive factors
Helicobacter pylori, also known as H. pylori
(cont’d)
• 60%–70% of patients with PUD have H. pylori infection
• H. pylori may also promote gastric cancer
• Duodenal ulcers are much more common among people
with H. pylori infection than among people who are not
infected
• Eradication of the bacterium promotes healing of the
PUD and minimized recurrence of PUD
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Pathogenesis of Peptic Ulcers
Aggressive factors
Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Inhibit the biosynthesis of prostaglandins
• Decrease blood flow, mucus, and bicarbonate
Gastric acid
• Causes ulcers by directly injuring cells of the GI mucosa
and indirectly by activating pepsin
• Increased acid alone does not increase ulcers but is a
definite factor in PUD
Pepsin
• Proteolytic enzyme in gastric juice
Smoking
• Delays ulcer healing and increases risk for recurrence
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Pathogenesis of Peptic Ulcers
Summary of ulcer development
Most common cause
• Infection with H. pylori (HP) is the most common cause of
gastric and duodenal ulcers
• Additional factors must be involved: 50% harbor HP,
but only 10% develop PUD
Second most common cause
• NSAIDs
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Overview of Treatment
Goals of drug therapy
Alleviate symptoms
Promote healing
Prevent complications
Prevent recurrence
Drugs do not alter the disease process; they
create conditions conducive to healing
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Classes of Antiulcer Drugs
Antibiotics
Antisecretory agents
Mucosal protectants
Antisecretory agents that enhance mucosal
defenses
Antacids
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Three Ways Antiulcer Drugs Work
Eradicate H. pylori
(antibiotics)
Reduce gastric acidity
(antisecretory agents, misoprostol)
Enhance mucosal defenses
(sucralfate, misoprostol)
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Drug Selection: H. pylori–
Associated Ulcers
Antibiotics
Should be given to all patients with
gastric/duodenal ulcers and documented H. pylori
Antisecretory agents
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Drug Selection: NSAIDInduced Ulcers
Prophylaxis
Risk factors for ulcer development (older than 60
years, history of ulcers, high-dose NSAID therapy)
Treatment
Proton pump inhibitors (PPIs) (eg, omeprazole)
are preferred
Misoprostol is also effective, but can cause
diarrhea
Antacids, sucralfate, and histamine2 receptor
blockers are not recommended
Discontinue NSAIDs, if possible
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Nondrug Therapy
Diet
Traditional “ulcer diet” does not accelerate healing
No convincing evidence indicates that caffeinated
beverages promote ulcers or delay healing
Change eating pattern to 5–6 small meals a day
(reduces pH fluctuations)
Avoid smoking, aspirin, other NSAIDs, and
alcohol if a trigger
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Evaluation of Therapy
Monitor for relief of pain
Keep in mind: cessation of pain and
disappearance of ulcer rarely coincide
Pain may subside before complete healing or may
continue after healing
Radiologic or endoscopic examination of
ulcer site
H. pylori tests
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H. pylori Tests
Noninvasive
Breath test
Serum test
Stool test
Invasive
Endoscopic specimen obtained and evaluated
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H. pylori Treatment
Minimum of two antibiotics (up to three)
prescribed to decrease risk of developing
resistance
Amoxicillin
Clarithromycin
Bismuth compounds
Tetracycline
Metronidazole
Tinidazole
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Antibiotic Regimen
2007 ACG updated guidelines for managing
H. pylori
Use minimum of two antibiotics, preferably three
Antisecretory agent (PPI, H2 antagonist)
Barriers to compliance
Can require up to 12 pills/day (14 days)
GI side effects
Expensive (about $200)
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Histamine2-Receptor Antagonists
Cimetidine (Tagamet)
Ranitidine (Zantac)
Famotidine (Pepcid)
Nizatidine (Axid)
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Histamine2-Receptor Antagonists
First-choice drugs for treating gastric and
duodenal ulcers
Promote healing by suppressing secretion of
gastric acid
All four equally effective
Serious side effects uncommon
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Fig. 78–2. A model of the regulation of gastric acid secretion showing the actions of
antisecretory drugs and antacids.
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Cimetidine (Tagamet)
Pharmacokinetics
Absorption slowed if taken with meals
Crosses the blood-brain barrier with difficulty
May cause some CNS side effects
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Cimetidine (Tagamet)
Therapeutic uses
Gastric and duodenal ulcers
Gastroesophageal reflux disease (GERD)
Zollinger-Ellison syndrome
Aspiration pneumonitis
Heartburn, acid indigestion, and sour stomach
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Cimetidine (Tagamet)
Adverse effects
Antiandrogenic effects
CNS effects
Pneumonia
IV bolus: can experience hypotension and
dysrhythmias
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Ranitidine (Zantac)
Shares many properties of cimetidine
More potent, fewer adverse effects, causes fewer
drug interactions than cimetidine (and has less
ability to cross CNS)
Adverse effects
Significant ones uncommon
Does not bind to androgen receptors
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Ranitidine (Zantac)
Therapeutic uses
Short-term treatment of gastric/duodenal ulcers
Prophylaxis of recurrent duodenal ulcers
Treatment of Zollinger-Ellison syndrome and
hypersecretory states
Treatment of GERD
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Famotidine (Pepcid)
Actions similar to those of ranitidine
Therapeutic uses
Short-term treatment of gastric/duodenal ulcers
Prophylaxis of recurrent duodenal ulcers
Treatment of Zollinger-Ellison syndrome and
hypersecretory states
Treatment of GERD
Over-the-counter (OTC): to treat heartburn, acid
indigestion, sour stomach
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Famotidine (Pepcid)
Adverse effects
Does not bind to androgen receptors
Possible increased risk for pneumonia caused by
elevation of pH
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Nizatidine (Axid)
Actions much like those of ranitidine and
famotidine
Therapeutic uses
Duodenal/gastric ulcers
GERD, heartburn, acid indigestion, and sour
stomach
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Proton Pump Inhibitors
Most effective drugs for suppressing secretion of
gastric acid
Therapeutic uses: short term
Gastric/duodenal ulcers
GERD
Well tolerated
Selection of PPI based on cost and prescriber
preference
Can increase the risk of serious adverse events,
including fracture, pneumonia, acid rebound, and
possibly intestinal infection with Clostridium difficile
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Omeprazole (Prilosec)
First available proton pump inhibitor
Actions and characteristics
Inhibits gastric secretion
Short half-life
Used for short-term therapy
Adverse effects
Usually inconsequential with short-term use
Headache
Gastrointestinal effects
Pneumonia
Rebound acid hypersecretion
C. difficile infection
Gastric cancer
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Other PPIs
Dexlansoprazole
Rabeprazole
Pantoprazole
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Other Antiulcer Drugs
Sucralfate (Carafate)
Misoprostol (Cytotec)
Antacids
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Sucralfate (Carafate)
Creates a protective barrier up to 6 hours
Therapeutic uses
Adverse effects
Acute ulcers and maintenance therapy
Constipation (in only 2% of patients)
Drug interactions
Minimal
Antacids may interfere with effects of sucralfate
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Misoprostol (Cytotec)
Therapeutic uses
Only approved GI indication is prevention of
gastric ulcers caused by long-term NSAID therapy
Adverse effects
Most common: dose-related diarrhea (13%–40%)
and abdominal pain (7%–20%)
Contraindicated during pregnancy: category X
• Significant actions need to be taken to ensure that
pregnancy does not occur after therapy starts, and that
patient is not pregnant at therapy initiation
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Antacids
React with gastric acid to produce neutral
salts or salts of low acidity
Decrease destruction of the gut wall by
neutralizing acid
May also enhance mucosal protection by
stimulating production of prostaglandins
Except for sodium bicarbonate, antacids do
not alter systemic pH
Use with caution in patients with renal
impairment
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