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PEPTIC ULCER DISEASE

Lecturer prof. Yu.R. Kovalev

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DEFINITION AND CLASSIFICATION

Peptic ulcer is a chronic cyclic disease with


periodic ulcerating lesions affecting the upper
gastro-intestinal tract.
•chronic duodenal ulcer
•chronic gastric ulcer
•anastomotic ulcer

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ETIOLOGY
Three major causes of peptic ulcer disease
are now recognized:
•NSAIDs,
•chronic H. pylori infection,
•acid hypersecretory states
Up to one-fourth of ulcers are idiopathic. Ulcers are
more common in smokers and in patients taking
NSAIDs on a chronic basis. Alcohol and dietary
factors do not appear to cause ulcer disease. The
role of stress is uncertain.
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ROLE OF NSAIDs
Users of NSAIDs are at least three times more likely
than nonusers to suffer serious gastrointestinal
complications from these ulcers such as bleeding or
perforation. Approximately 1-2% of chronic NSAID
users will have a major complication within 1 year.
Aspirin is the most ulcerogenic NSAID. The risk
appears to be dose-related, with some risk even at
doses as low as 81 mg every other day. The relative
risk of gastric ulcers is increased 40-fold, but the
risk of duodenal ulcers is only slightly increased.

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ROLE OF H. PYLORI
H. pylori appears to be a necessary cofactor for the
majority of duodenal and gastric ulcers. The
prevalence of H. pylori infection in duodenal ulcer
patients is about 70-75%. One in six infected patients
will develop ulcer disease.
Many H. pylori-infected patients have increased
gastric acid secretion. It is hypothesized that
increased acid exposure can engender small islands
of gastric metaplasia in the duodenal bulb.
Colonization of these islands by H. pylori may lead
to duodenitis or duodenal ulcer.
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HELICOBACTER PYLORI

It’s S-shaped and contains multiple flagella.


Key factors: urease, catalase, lipase,
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plateled-activating factor, vacuolating cytotoxine.
HELICOBACTER
PYLORIHELICOBACTER PYLORI

Electronic microscopy
Australian doctor who found out H.P.
got Nobel Price last year. 7
RISK FACTORS FOR H.P.
•Birth or residence in a developing country
•Low socioeconomic status
•Domestic crowding
•Unsanitary living conditions
•Unclean food or water

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PATHOGENESIS
AGGRESSIVE FACTORS
•H+
•Pepsin
COMPONENTS OF DEFENSE AND REPAIR
Preepithelial
•Mucose (mucous gel)
•Bicarbonate
•Surface active phospholipids

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PATHOGENESIS
COMPONENTS OF DEFENSE AND REPAIR
Epithelial
•Cellular resistance
•Restitution
•Growth factors (epidermal, transforming a.o.)
•Prostaglandins
Subepithelial
•Blood flow
•Microcirculation

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Components involved in providing
gastroduodenal mucosal defense and repair

Gastric gland 11
Potential long-term consequences of H.
pylori infection

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Mechanisms by wich NSAIDs may
induce mucosal injury

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CLINICAL FEATURES
Pain is typically localized to the epigastrium and
not severe. It is described as gnawing, dull, aching,
or "hunger-like." Approximately half of patients
report relief of pain with food or antacids
(especially duodenal ulcers) and a recurrence of
pain 2-4 hours later. Two-thirds of duodenal ulcers
and one-third of gastric ulcers cause nocturnal pain
that awakens the patient.

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CLINICAL FEATURES
A change from a patient's typical rhythmic
discomfort to constant or radiating pain may reflect
ulcer penetration or perforation. Most patients have
symptomatic periods lasting up to several weeks
with intervals of months to years in which they are
pain-free (periodicity).
Twenty percent of patients with ulcer complications
such as bleeding have no antecedent symptoms
("silent ulcers").

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CLINICAL FEATURES
Nausea and anorexia may occur with gastric
ulcers. Significant vomiting and weight loss
are unusual with uncomplicated ulcer disease
and suggest gastric outlet obstruction or
gastric malignancy.
The physical examination is often normal in
uncomplicated peptic ulcer disease. Mild,
localized epigastric tenderness to deep
palpation may be present. Fecal occult blood
testing is positive in one-third of patients.
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LABORATORY FINDINGS
Anemia may occur with acute blood loss from
a bleeding ulcer or less commonly from
chronic blood loss. Leukocytosis suggests
ulcer penetration or perforation. An elevated
serum amylase in a patient with severe
epigastric pain suggests ulcer penetration
into the pancreas.

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ENDOSCOPY
Endoscopy provides better diagnostic
accuracy than barium radiography and the
ability to biopsy for the presence of
malignancy and H. pylori infection. Duodenal
ulcers are virtually never malignant and do
not require biopsy. Three to 5 percent of
benign-appearing gastric ulcers prove to be
malignant.
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IMAGING
Barium upper gastrointestinal series is an
acceptable alternative to screening of
uncomplicated patients with dyspepsia.
However, because it has limited accu-racy in
distinguishing benign from malignant gastric
ulcers, all gastric ulcers diagnosed by x-ray
should be reevaluated with endoscopy after 8-
12 weeks of therapy.

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H. PYLORI TESTING
In patients in whom an ulcer is diagnosed by
endoscopy, gastric mucosal biopsies should be
obtained for a rapid urease test. Alternatively,
serologic testing may be the most cost-effective
means of confirming H pylori infection.
In patients with a history of peptic ulcer or when an
ulcer is diagnosed by upper gastrointestinal series,
noninvasive assessment for H pylori with fecal
antigen assay, serologic testing, or urea breath
testing should be done.
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MANAGEMENT
The goals of treatment are to relieve dyspeptic
symptoms, to promote ulcer healing, and to
eradicate H pylori infection. Uncomplicated H pylori-
associated ulcers should be treated for the first 10-
14 days.
Patients should be encouraged to eat balanced
meals at regular intervals. There is no justification
for bland or restrictive diets. Moderate alcohol intake
is not harmful. Smoking retards the rate of ulcer
healing and increases the frequency of recurrences
and should be discouraged.
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MANAGEMENT
The pharmacology of ulcers
• (1) acid-antisecretory agents,
• (2) mucosal protective agents,
• (3) agents that promote healing through
eradication of H pylori.

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Drugs used in the treatment of peptic
ulcer disease
Drug type/mechanism Examples Dose

Acid-suppressing drugs
Antacids Maalox, Tums, 100-140 meg/L
Gaviscon 1 and 3 h after
meals and hs
H2 receptor antagonists Cimetidine, 800 mg hs
Ranitidine, 300 mg hs
Famotidine 40 mg hs
Proton pump inhibitors Omeprazole, 20 mg/d
Lansoprazole, 30 mg/d
Rabeprasole 20 mg/d 23
Drugs used in the treatment of peptic
ulcer disease
Drug type/mechanism Examples Dose
Mucosal protective agents

Sucralfate Sucralfate 1 g qid

Prostaglandine analoque Misoprostol 200 mg qid

Bismuth-containing Bismuth
compounds subsalicylate
(BSS)

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HELICOBACTER PYLORY
ERADICATION THERAPY
•Omeprasoli 20 mg twice daily or Ranitidine
400 mg twice daily
•Bismuth subcitrate (De-Nol) two tablets four
times daily
•Tetracyclini 500 mg four times daily
Metronidazoli 250 mg four times daily

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HELICOBACTER PYLORY
ERADICATION THERAPY
The most common triple therapy
•Omeprasol (lanzoprazol) 20 mg bid
•Clarithromycin 500 mg bid
•Amoxicillin 1 g bid
for 14 days
In the absence of eradication of Hp –
recurrence of PU within one year 85%.
After succesful eradication – 5%-20% within
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one year.

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