Download Peptic Ulcer Disease (PUD)

Ahmad Hormati
Assistant Professor of Gastroenterology
Qom University of Medical Sciences.
Email: [email protected]
http://hormatigi.ir
PEPTIC ULCER DISEASE
Objectives
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Definition of peptic ulcer
Comparison of duodenal & gastric ulcers
etiology
Clinical presentation
Management
Emergency scenario
What is a peptic ulcer?
Peptic Ulcer Disease (PUD)
Definition
Peptic ulcer
refers to erosion of the mucosa lining any portion of the G.I. tract.
It is defined as : A circumscribed ulceration of the gastrointestinal mucosa
occurring in areas exposed to acid and pepsin and most often caused by
Helicobacter pylori infection. (Uphold & Graham, 2003)
gastric ulcer : the ulcer that occurs in the stomach lining ,some of them may
be malignant
duodenal ulcer : most often seen in first portion of duodenum (>95%)
Normal
Esophagus & Stomach
Peptic Ulcer Disease
Pathogenesis :
Protective factors vs. hostile factors
Etiology of PUD
A) Normal
B) Increased Attack
*Hyperacidity
*Pepsin.
*NSAIDs.
C) Weak defense
*Helicobacter pylori
*Stress, drugs, smoking
Peptic ulcer disease
Peptic Ulcer Disease
Pathogenesis :
Alarm symptoms
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In addition to increasing age, the following "alarm
symptoms" raise the suspicion of gastric malignancy, although
their accuracy in predicting or excluding malignancy remains
unsettled :
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Unintended weight loss
Persistent vomiting
Progressive dysphagia
Odynophagia
Otherwise unexplained anemia or iron deficiency
Hematemesis
Palpable abdominal mass or lymphadenopathy
Family history of upper gastrointestinal cancer
Previous gastric surgery
Jaundice
Duodenal Ulcer Vs. Gastric Ulcer
 duodenal sites are 4x as common as common in late middle age.
incidence increases with age.
gastric sites
 most common in middle age with Male to female ratio—2:1
More common with bl. group A
peak 30-50 years
 Male to female ratio—4:1
Use of NSAIDs: associated with a
 Genetic link: 3x more common in 1st three- to four-fold increase in risk of
degree relatives
gastric ulcer
 more common with blood group O
 associated
with
increased
Less related to H. pylori than
serum duodenal ulcers : about 80%
pepsinogen
10 - 20% of patients with a gastric
 H. pylori infection common,up to 95%
ulcer have a concomitant duodenal
 smoking is twice as common
ulcer
Duodenal vs Gastric
DUODENAL
GASTRIC
INCIDENCE
More common
Less common
ANATOMY
First part of duodenum –
anterior wall
Lesser curvature of stomach
DURATION
Acute or chronic
Chronic
MALIGNANCY
Rare
Benign or malignant
Peptic Ulcer Disease
Causes:
The causes of peptic ulcer disease include the following:
 Infection with the bacteria Helicobacter pylori occurs in 80 to 95% of patients
with peptic ulcer disease. H. pylori infection impairs the protective mechanisms of the
G.I. tract against low pH and digestive enzymes and leads to ulceration of the
mucosa.
 Stress — Emotional, trauma, surgical.
 Injury or death of mucus-producing cells.
 Excess acid production in the stomach. The hormone gastrin stimulates the
production of acid in the stomach; therefore, any factors that increase gastrin
production will in turn increase the production of stomach acid.
Drugs: Chronic use of aspirins and NSAIDs, or Corticosteroids
Risk factors
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HELICOBACTER PYLORI
Non Steroidal Anti-inflammatory Drugs
Steroid therapy
Smoking
Excess alcohol intake
Genetic factors
Zollinger Ellison syndrome – rare syndrome caused by
gastrin-secreting tumour
Blood group O
Hyperparathyroidism
H Pylori
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Urease producing, gram negative bacillus
Developing countries
Infection increases with age
Infects mucosa of stomach > inflammatory response
> gastritis > increased gastrin secretion > gastric
metaplasia > damage to mucosa > ulceration
Increased risk of developing gastric
adenocarcinoma
Helicobacter pylori:
 Most common infection in the world (20%)
 10% of men, 4% women develop PUD
 Positive in 70-100% of PUD patients.
No acid
No ulcer
 H.pylori related disorders:
 Chronic gastritis – 90%
 Peptic ulcer disease – 95-100%
 Gastric carcinoma – 70%
OLD TESTAMENT
 Gastric lymphoma
 Reflux Oesophagitis.
 Non ulcer dyspepsia
No HP
No ulcer
NEW TESTAMENT
Helicobacter pylori:
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Gram negative, Spiral bacilli
Spirochetes
Do not invade cells – only mucous
Breakdown urea - ammonia
Break down mucosal defense
Chronic Superficial inflammation
H pylori testing
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C urea breath tests
Stool antigen tests
Serology
Endoscopy with biopsy
Urease Breath Test.
Differential diagnoses for epigastric
pain
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Surgical
 Biliary
colic, acute cholecystitis
 Pancreatitis
 Perforation of viscus
 Acute appendicitis
 Malignancy
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Medical
 GORD
 MI
 PE
 Pneumonia
Symptoms of PUD
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Asymptomatic
Epigastric pain
Nausea
Oral flatulence, bloating, distension and intolerance
of fatty food
Heartburn
Pain radiating to the back
ALARM signs for epigastric pain
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Chronic GI bleeding
Iron-deficiency anaemia
Progressive unintentional weight loss
Progressive dysphagia
Persistent vomiting
Epigastric mass
Patients aged 55 years and older with unexplained
and persistent recent- onset dyspepsia alone
Peptic Ulcer Disease
Manifestations:
Manifestations of peptic ulcer disease:
• Episodes of remission and exacerbation
• Pain that for duodenal ulcers is often relieved by eating or
antacids
• G.I. bleeding and possible hemorrhage (20 to 25% of
patients)
• Perforation of ulcers with significant mortality
• Obstruction of G.I. tract
PUD - Diagnosis
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Endoscopy
Barium meal – contrast x-ray
Biopsy – bacteria & malignancy
H.Pylori:
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Endoscopy cytology
Biopsy – Special stains
Culture - difficult
Urease Breath test.
PUD – Complications
 Bleeding – Chronic, Acute, Massive
 Fibrosis, Stricture obstruction – pyloric stenosis.
 Perforation – Peritonitis- emergency.
 Gastric carcinoma. (not duodenal carcinoma)
Non-pharmacological Treatment of Peptic
ulcer
1-Avoid spicy food.
2-Avoid xanthin containing beverges.
3-Avoid Alcohol.
4-Avoid Smoking.
5-Avoid heavy meals.
6-Encourage small frequent low caloric meals.
7-Avoid
ulcerating
drugs
e.g.
NSAIDs,
corticosteroids,
xanthines
and
parasympathomimetics
PUD –Treatment
Triple therapy for 14 days is considered the ttt of choice.
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Proton Pump Inhibitor + clarithromycin and amoxicillin
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Omeprazole (Prilosec): 20 mg PO bid for 14 d or
Lansoprazole (Prevacid): 30 mg PO bid for 14 d or
Rabeprazole (Aciphex): 20 mg PO bid for 14 d or
Esomeprazole (Nexium): 40 mg PO qd for 14 d plus
Clarithromycin (Biaxin): 500 mg PO bid for 14 and
Amoxicillin (Amoxil): 1 g PO bid for 14 d
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Can substitute Flagyl 500 mg PO bid for 14 d if allergic to Penicillin.
In the setting of an active ulcer, continue on proton pump inhibitor therapy for additional
2 weeks.
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Goal: complete elimination of H. Pylori. Once achieved reinfection rates are low.
FUNCTIONAL
DYSPEPSIA
DEFINITION
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An international committee of clinical investigators developed the
following revised definition (Rome III criteria) of functional dyspepsia
for research purposes, which can also be applied to clinical practice:
One or more of:
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AND
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Bothersome postprandial fullness
Early satiation
Epigastric pain
Epigastric burning
No evidence of structural disease (including at upper endoscopy) that is
likely to explain the symptoms.
These criteria should be fulfilled for the last three months with
symptom onset at least six months before diagnosis.
Treatment
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We suggest patients be reassured and given dietary
and psychosocial advice as needed (Grade 2C).
We suggest that patients who do not respond to the
above be given a trial of acid suppression (Grade
2B).
The benefit of acid suppression may be greatest in
those who have reflux-like symptoms. We suggest a
four- to eight-week trial of a proton pump inhibitor
Treatment
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H. pylori eradication benefits only a minority of
patients.
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Guidelines issued by the American Gastroenterological
Association and the American College of
Gastroenterology recommend H. pylori eradication in
patients with functional dyspepsia emphasizing a possible
short-term benefit (number needed to treat around 17) and
a possible long-term benefit
However, because of potential side effects of therapy, we
suggest the decision to eradicate H. pylori consider the
individual patient's clinical features, including response to
other therapy and psychological factors (Grade 2B).
Treatment
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Some patients may respond to an antidepressant drug.
We suggest an antidepressant trial for patients in
whom PPI therapy has failed, especially if there is
insomnia, which might also respond (Grade 2C).
We generally use a tricyclic antidepressant drug or
trazodone, starting with a low dose (eg,
amitriptyline 10 mg at bedtime, desipramine 25 mg at
bedtime, or trazodone 25 mg at bedtime) and
increasing after a few days, usually to only two or three
times these doses.
Treatment
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Prokinetics can occasionally help.
However, access to cisapride is highly restricted in the United
States and many other countries. Domperidone is not
marketed in the United States and metoclopramide often
causes side effects.
We generally limit a trial of metoclopramide (5 to 10 mg
three times daily one-half an hour before meals and at
night for about four weeks) to young patients in whom other
therapies have failed.
Herbal therapies continue to be investigated; we do not use
them.
Rockall score