Socioeconomic status may play into risk factors as well.
In both types of peptic ulceration, gastric and duodenal, there is an imbalance between secretion and neutralization of secreted acid. In duodenal ulcers there is an oversecretion of acid whilst in gastric ulcers there is an impairment of mucosal protection
Peptic Ulcer Disease Dr Shatdal
Peptic Ulcer Disease
Dr. Shatdal Chaudhary
Assistant Professor (Internal Medicine)
B.P. Koirala Institute of Health Sciences,
An ulce r is defined as disruption of the
mucosal integrity leading to a local defect or
excavation due to active inflammation
Erosion: Damage within the mucosal layer
Ulce rs are defined as breaks in the mucosal
surface >5 mm in size, with depth to the
The term 'peptic ulcer' refers to an ulcer in the
lower oesophagus, stomach or duodenum, in
the jejunum after surgical anastomosis to the
stomach or, rarely, in the ileum adjacent to a
Gastroduodenal Mucosal Defense
• 3-level barrier preepithelial, epithelial, and
• Mucus-bicarbonate layer serves as a
• Surface epithelial cells provides defense
epithelial cell ionic transporters that maintain
intracellular pH and HCO3 production
intracellular tight junctions
Gastroduodenal Mucosal Defense
Role of Prostaglandins
Gastric mucosa contains abundant levels of
Play central role in epithelial defense/repair
Regulate release of mucosal HCO3 & mucus
Inhibit parietal cell secretion
Maintain mucosal blood flow
Epithelial cell restitution.
duodenal sites are 4x as common as gastric sites
most common in middle age
peak 30-50 years
Male to female ratio—5:1
Genetic link: 3x more common in 1st
more common in patients with blood group O
associated with increased serum pepsinogen
H. pylori infection common
up to 95%
smoking is twice as common
common in late middle age
incidence increases with age
Male to female ratio—2:1
More common in patients with blood group A
Use of NSAIDs - associated with a three- to four-fold
increase in risk of gastric ulcer
Less related to H. pylori than duodenal ulcers – about
10 - 20% of patients with a gastric ulcer have a
concomitant duodenal ulcer
1982- Waren and Marshall described first-named
1985: Association with peptic ulcer
1989: Named as ‘helicobacter ‘(helico-curved; bacter-staff)
• H. pylo ri inf. is virtually always associated with
chronic active gastritis.
• But only 10–15% develop frank PUD.
Tolerance of the acid conditions (pH 1-2)
1. Urease: urea -> CO2 + NH3,
then NH3 + H+ -> NH4+, which
2. Residence in mucus and on the
3. Capacity to create an ionic
gradient at a low pH.
4. Release of factors that
decrease acid secretion by
parietal cells during early
• H. pylori is able to fight off the stomach acid that does reach it
with the enzyme urease.
• Urease converts urea into bicarbonate and ammonia, which
are strong bases.
• These acid neutralizing chemicals
around the H. pylori protect if from
the acid in the stomach.
• AThe most important contributing factors are
H pylori, NSAIDs, acid, and pepsin.
• Additional aggressive factors include smoking,
ethanol, bile acids, aspirin, steroids, and
• Important protective factors are mucus,
bicarbonate, mucosal blood flow,
prostaglandins, hydrophobic layer, and
– Increased risk when older than 50 d/t decrease
Causes of Ulcers Not Caused by Hp and
Herpes simplex virus Basophilia in myeloproliferative disease
He lico bacte r he ilm anni Duodenal obstruction (e.g., annular
Drug/Toxin Infiltrating disease
combined with NSAIDs)
Potassium chloride Crohn's disease
Mycophenolate mofetil Idiopathic hypersecretory state
Clinical Features : DU
Typical pain pattern in DU occurs 90 min to 3
h after meal and is relieved by antacids or
Awakes the patient from sleep : the most
discriminating symptom( 2/3rd of DU pt.)
Unfortunately, this symptom also present in
of patients with NUD.
Clinical Features: GU
Pain pattern in GU may be different
Precipitated by food.
While vomiting relieves it.
Nausea and weight loss occur more
commonly in GU patients.
Mechanism of pain in ulcer is unknown.
Possible explanations include
acid-induced activation of chemical receptors
in the duodenum
enhanced duodenal sensitivity to bile acids
and pepsin, or
altered gastroduodenal motility
Guaic-positive stool resulting from occult blood loss
Succussion splash resulting from scaring or edema
due to partial or complete gastric outlet obstruction
A succussion splash describes the sound obtained by
shaking an individual who has free fluid and air or gas in a
hollow organ or body cavity.
Usually elicited to confirm intestinal or pyloric obstruction.
Done by gently shaking the abdomen by holding either
side of the pelvis. A positive test occurs when a splashing
noise is heard, either with or without a stethoscope. It is
not valid if the pt has eaten or drunk fluid within the last
Neoplasm of the stomach
Nonulcer dyspepsia (also called functional dyspepsia)
MI—not to be missed if having chest pain
Poor predictive value of abdominal pain for the
presence of a gastroduodenal ulcer
Multiple disease that can mimic this disease
Most patients with symptoms s/o an ulcer
Empirical therapy is appropriate for pts who
are otherwise healthy and <45, before
embarking on a diagnostic evaluation .
Diagnostic Evaluation Barium studies
• Sensitivity for detecting
single-contrast Ba meals
• Sensitivity decreased in
small ulcers (<0.5 cm),
presence of previous
scarring, or in postop
Most sensitive and specific .
Direct visualization of the mucosa,
Biopsy to rule out malignancy or Hp.
Identifies lesions too small to detect by Ba
exam, for evaluation of atypical radiographic
abnormalities, or to determine if an ulcer is a
source of blood loss.
Tests for Detection of H. pylori
Invasive (Endoscopy/Biopsy Required)
Rapid urease 80–95/95–
Simple, false negative with recent use of PPIs,
antibiotics, or bismuth compounds
Histology 80–90/>95 provides histologic information
Culture —/— Time-consuming, expensive ; antibiotic
Serology >80/>90 Inexpensive, convenient; not useful for early
>90/>90 Simple, rapid; useful for early follow-up; false
negatives with recent therapy ; exposure to low-
dose radiation with 14
Stool antigen >90/>90 Inexpensive, convenient; not established for
eradication but promising
• H. Pylori Positive: retesting for tx efficacy
• Urea breath test—no sooner than 4 weeks after
therapy to avoid false negative results
• Stool antigen test—an 8 week interval must be allowed
• H. Pylori Negative:
• evaluate symptoms after one month. Patients who are
controlled should cont. 2-4 more weeks.
1. Medically refractory disease: rare
2. Treatment of an ulcer-related complication
Specific Operations for Duodenal
1. Vagotomy and drainage (by
2. Highly selective vagotomy
(which does not require a
3. Vagotomy with antrectomy
Severe peptic ulcer diathesis secondary to
gastric acid hypersecretion due to unregulated
gastrin release from a non- β cell endocrine
Incidence varies from 0.1 to 1% of individuals
presenting with PUD.
Males > females,
Ages 30 and 50 yrs.
Gastrinomas are classified into sporadic tumors
(more common) and those associated with MEN
ZES: Clinical Manifestations
Peptic ulcer is the most common clinical
in unusual locations (D2 & beyond)
refractory to standard medical therapy
recurrence after acid-reducing surgery
presenting with frank complications
in the absence of H. pylo ri or NSAID .
ZES: Clinical Manifestations
Diarrhea, found in up to 50%.
Gastrinomas can develop in the presence of
MEN I syndrome in ~25% of patients.
AD disorder involves primarily 3 organs:
parathyroid glands (80–90%), pancreas (40–
80%), and pituitary gland (30–60%).
PPIs are the treatment of choice