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10 Peptic Ulcer Intro
10 Peptic Ulcer Intro
10 Peptic Ulcer Intro
PATHOPHYSIOLOGY
The normal stomach maintains a balance between protective factors, such as mucus
and bicarbonate secretion, and aggressive factors, such as acid secretion and pepsin.
Gastric ulcers develop when aggressive factors overcome protective mechanisms.
The two major etiological factors for PUD are Helicobacter pylori infection and
nonsteroidal anti-inflammatory drug (NSAID) consumption. Currently, 70% of all
gastric ulcers occurring in the United States can be attributed to H pylori infection.
In addition to an increase in acid secretion, H pylori infection also predisposes
patients to ulcer disease by disrupting mucosal integrity. The bacterium's spiral shape
and flagella facilitate its penetration into the mucous layer and its attachment to the
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epithelial layer. Subsequently, it releases phospholipase and proteases, which cause
further mucosal damage.
Helicobacter NSAID
pylori
Gastrinoma
↑Serum
Chronic Blocks Gastrin
Active COX-1
Gastritis
ECL Cell Histamine
↓PGs Release
Peptic Ulcer
Disease HCl, Pepsin Hyper
(More Duodenal Peptic Ulcer secretion
than Gastric) Disease
(More Gastric
than Duodenal) Peptic Ulcer Disease
(Much More Duodenal than
Gastric
(a) (b) (c)
(a) Helicobacter pylori induces a diffuse, chronic, active superficial gastritis,
usually throughout the stomach (b) Nonselective nonsteroidal anti-inflammatory
drugs (NSAIDs) (c) Gastrinoma cells
figure 1.3a: pathogenesis of peptic ulcer
NSAID-induced ulcers account for approximately 26% of gastric ulcers, and they
are believed to be secondary to a decrease in prostaglandin production resulting from
the inhibition of cyclooxygenase. COX-2 selective NSAIDs produce a lesser
reduction in prostaglandins and are associated with fewer peptic ulcers than non
selective COX-1. The greatest risk of developing an ulcer occurs during the first 3
months of NSAID use; thereafter, the risk decreases but continues to be present.
Whether concurrent H pylori infection and NSAID use are synergistic in producing
gastric ulcers remains unclear. Recent accumulating evidence indicates that patients
with H pylori infection may be twice as likely to get a bleeding peptic ulcer.
A rare cause of PUD is Zollinger-Ellison syndrome (ie, Gastrinoma). The hallmark
of Zollinger-Ellison syndrome is the profound hyper secretion of gastric acid.
Gastrinoma cells in the pancreas or duodenum secrete large amounts of gastrin into
the circulation. Elevated serum gastrin levels promote the release of histamine by
acting on receptors for cholecystokininB (CCKB) and for gastrin, which are located
on gastric enterochromaffin-like (ECL) cells. Histamine acts on H2 receptors on
parietal and chief cells to augment hydrochloric acid (HCl) and pepsin secretion.
Significant disruption of the mucosal integrity often results in multiple duodenal and
gastric ulcers. (Feldman Mark.2005)
DIAGONOSIS
Tests used in the diagnosis of peptic ulcer are
• EGD • Hypotonic
(esophagogastroduodenoscopy duodenography
) • Urea breath test
• Diatrizoate sodium • Serologic ELISA
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• Urine-based ELISA and rapid urine test
• Endoscopic biopsy
• Stool antigen test
(Ramakrishnan K. 2007)
CLINICAL FEATURE
Table 1.3b: SYMPTOMS OF PEPTIC ULCER DISEASE
Duodenal Ulcer 1.Pain that awakens patients from sleep
symptoms: 2. Burning or gnawing sensation in the upper abdomen
3. Pain in the back, lower abdomen or chest area may
occasionally occur
4. Pain that occurs when the stomach is empty (about
two hours
After a mean or during the night). Relief frequently
occurs after eating
Gastric Ulcer symptoms 1. Gastric ulcer pain may be less severe than duodenal
ulcer pain and is noticeably higher in the abdomen
2. Eating may increase pain rather than relieve pain
3. Pain is described as aching, nagging, cramping or
dull
4. Other symptoms may include nausea, vomiting and
weight loss
Some ulcers may produce no symptoms at all. However, occasional painless bleeding,
anaemia or the passage of black, tarry stool may be the first sign of peptic ulcer
disease.
(Berardi RR, Welage LS. 2005)
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Table 1.3c: RISK FACTORS FOR PEPTIC ULCER
Established Risk Factors Possible Risk Factors Questionable Risk
Factors
• Age over 60 years • NSAIDs-related • Cigarette
• previous peptic ulcer dyspepsia smoking
disease • Duration of • Alcohol
• Previous upper GI NSAIDs use consumption
bleeding • Helicobacter
• Concomitant pylori infection
corticosteroid therapy • Rheumatoid
• high-dose and multiple arthritis
NSAIDs use
• Concomitant
anticoagulant use or
coagulopathy
• Chronic major organ
impairment (e.g.,
cardiovascular disease)
MANAGEMENT
DESIRED OUTCOME
The goals of treatment are relieving ulcer pain, healing the ulcer, preventing ulcer
recurrence, and reducing ulcer-related complications. In HP positive patients with an
active ulcer, a previously documented ulcer, or a history of an ulcer-related
complication, the goals are to eradicate the organism, heal the ulcer, and cure the
disease with a cost-effective drug regimen.
NONPHARMACOLOGIC TREATMENT
PHARMACOLOGIC TREATMENT
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Treatment duration is 10 to 14 days (although courses lasting one to seven days have
been reported to have Comparable effectiveness. eradication rates 80 to 90 percent or
higher.
• HISTAMINE H2 BLOCKERS
70 to 80 percent healing in duodenal ulcer after four weeks, 87 to 94 percent after eight
weeks.
• SUCRALFATE (CARAFATE)
Treatment duration is four weeks effectiveness.
• SURGERY
Rarely needed similar to H2 blockers.
Berardi RR, Welage LS.2005)
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Table 1.3d: Drug Regimens to Eradicate Helicobacter Pylori
Drug #1 Drug #2 Drug #3 Drug #4
Proton pump inhibitor–based three-drug regimens
Omeprazole 20 mg twice daily Clarithromycin 500 Amoxicillin 1 g twice
or Lansoprazole 30 mg twice mg twice Daily daily
daily or Metronidazole
or Pantoprazole 40 mg twice 500mg twice daily
daily
or Esomeprazole 40 mg daily
or Rabeprazole 20 mg daily
COMPLICATIONS
FOLLOW-UP
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