1. Peptic Ulcer Disease
Dr. Shatdal Chaudhary
Assistant Professor (Internal Medicine)
B.P. Koirala Institute of Health Sciences,
Dharan
2. An ulcer 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
Ulcers are defined as breaks in the mucosal
surface >5 mm in size, with depth to the
submucosa.
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
3.
4. Gastroduodenal Mucosal Defense
• 3-level barrier preepithelial, epithelial, and
subepithelial elements
• Mucus-bicarbonate layer serves as a
physicochemical barrier
• Surface epithelial cells provides defense
mucus production,
epithelial cell ionic transporters that maintain
intracellular pH and HCO3 production
intracellular tight junctions
5. Gastroduodenal Mucosal Defense
Role of Prostaglandins
Gastric mucosa contains abundant levels of
PG
Play central role in epithelial defense/repair
Regulate release of mucosal HCO3 & mucus
Inhibit parietal cell secretion
Maintain mucosal blood flow
Epithelial cell restitution.
7. Duodenal Ulcers
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 degree relatives
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
8. Gastric Ulcers
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
70%
10 - 20% of patients with a gastric ulcer have a
concomitant duodenal ulcer
9. H. Pylori
HISTORY
1982- Waren and Marshall described first-named
“campylobacter pyloridis”
1985: Association with peptic ulcer
1989: Named as ‘helicobacter ‘(helico-curved; bacter-staff)
10. Pathophysiology
• H. pylori inf. is virtually always associated with
chronic active gastritis.
• But only 10–15% develop frank PUD.
12. Pathophysiology
Tolerance of the acid conditions (pH 1-2)
1. Urease: urea -> CO2 + NH3,
then NH3 + H+ -> NH4+, which
provides buffering.
2. Residence in mucus and on
the epithelial cells.
3. Capacity to create an ionic
gradient at a low pH.
4. Release of factors that
decrease acid secretion by
parietal cells during early
infection.
13. • 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.
15. Etiology
• AThe most important contributing factors are
H pylori, NSAIDs, acid, and pepsin.
• Additional aggressive factors include smoking,
ethanol, bile acids, aspirin, steroids, and
stress.
• Important protective factors are mucus,
bicarbonate, mucosal blood flow,
prostaglandins, hydrophobic layer, and
epithelial renewal.
– Increased risk when older than 50 d/t decrease
protection
16. Causes of Ulcers Not Caused by Hp and
NSAIDs
Infection Miscellaneous
Cytomegalovirus,
Herpes simplex virus Basophilia in myeloproliferative disease
Helicobacter heilmanni Duodenal obstruction (e.g., annular
pancreas)
Drug/Toxin Infiltrating disease
Bisphosphonates Ischemia
Glucocorticoids (when combined
with NSAIDs)
Radiation therapy
Chemotherapy Sarcoidosis
Potassium chloride Crohn's disease
Mycophenolate mofetil Idiopathic hypersecretory state
17. Clinical Features : DU
Abdominal pain
Typical pain pattern in DU occurs 90 min to 3 h
after meal and is relieved by antacids or food.
Awakes the patient from sleep : the most
discriminating symptom( 2/3rd of DU pt.)
Unfortunately, this symptom also present in
1/3rd of patients with NUD.
18. 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.
19. Clinical features
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
20. On Examination
Epigastric tenderness
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
three hours.
21. Differential Diagnosis
Neoplasm of the stomach
Pancreatitis
Pancreatic cancer
Diverticulitis
Nonulcer dyspepsia (also called functional dyspepsia)
Cholecystitis
Gastritis
GERD
MI—not to be missed if having chest pain
23. Diagnostic Evaluation
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 have
NUD;
Empirical therapy is appropriate for pts who
are otherwise healthy and <45, before
embarking on a diagnostic evaluation .
24. Diagnostic Evaluation Barium studies
• Sensitivity for detecting
a DU
single-contrast Ba meals
80%: double-contrast
90%.
• Sensitivity decreased in
small ulcers (<0.5 cm),
presence of previous
scarring, or in postop
pt.
25. Endoscopy
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.
26. Tests for Detection of H. pylori
Test Sensitivity/Sp
ecificity, %
Comments
Invasive (Endoscopy/Biopsy Required)
Rapid urease 80–95/95–
100
Simple, false negative with recent use of PPIs,
antibiotics, or bismuth compounds
Histology 80–90/>95 provides histologic information
Culture —/— Time-consuming, expensive ; antibiotic
susceptibility
Non-invasive
Serology >80/>90 Inexpensive, convenient; not useful for early
follow-up
Urea breath
test
>90/>90 Simple, rapid; useful for early follow-up; false
negatives with recent therapy ; exposure to low-
dose radiation with 14C test
Stool antigen >90/>90 Inexpensive, convenient; not established for
eradication but promising
30. Evaluation/Follow-up/
• 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
after therapy.
• H. Pylori Negative:
• evaluate symptoms after one month. Patients who are
controlled should cont. 2-4 more weeks.
32. Specific Operations for Duodenal
Ulcers
1. Vagotomy and drainage (by
pyloroplasty,
gastroduodenostomy, or
gastrojejunostomy),
2. Highly selective vagotomy
(which does not require a
drainage procedure)
3. Vagotomy with antrectomy
33. Zollinger–Ellison Syndrome
Severe peptic ulcer diathesis secondary to
gastric acid hypersecretion due to unregulated
gastrin release from a non- β cell endocrine
tumor (gastrinoma)
34. Zollinger–Ellison Syndrome
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
type I
35. ZES: Clinical Manifestations
Peptic ulcer is the most common clinical
manifestation
Suspicious Ulcers
in unusual locations (D2 & beyond)
refractory to standard medical therapy
recurrence after acid-reducing surgery
presenting with frank complications
in the absence of H. pylori or NSAID .
36. 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%).
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