Peptic Ulcer Disease is caused by an imbalance between aggressive factors like acid and pepsin and protective mucosal defenses. The most common sites are the duodenum and stomach. Risk factors include H. pylori infection, NSAID use, smoking, stress, and Zollinger-Ellison syndrome. Patients present with epigastric pain, nausea, bleeding, or anemia. Endoscopy is the gold standard for diagnosis and allows visualization of ulcers. Treatment involves eradicating H. pylori if present, prescribing PPIs, and surgery for complications like bleeding or perforation. Complications can include bleeding, perforation, penetration, and malignant transformation if not properly treated.

1. Peptic Ulcer Disease
Dr. Sachit Koirala [Resident, 1st Year]
Facilitator : Dr. Mahipendra Tiwari
KIST Medical College
Lalitpur Nepal
2078-04-31

2. Introduction
• Peptic ulcers : Focal defects in the gastric or duodenal mucosa that extend into
the submucosa or deeper.
• ‘Peptic’ : Associated with Pepsin
• But, Peptic Ulcer Disease (PUD) does not occur in the absence of acid
• Responsible for up to two-thirds of upper GI bleed
• imbalance between mucosal barriers and other aggravating factors
• Common sites : Duodenum and lesser curvature of stomach
• Less common sites : Esophagus, Meckel diverticulum

4. Arterial supply to stomach

5. Vagal nerve supply to stomach

6. M : Muscarinic receptor ECL : Enterochromaffin Like
H : Histamine receptor
G : Gastrin receptor

7. Pathogenesis

9. H. pylori
• 77% of duodenal ulcers are associated with H. pylori infection
• Gram –ve spiral like flagellated organism, first studied by Warren and Marshall
(both got Nobel prize)
• No. 1 carcinogen in Gastric Carcinoma
• Releases Urease  Urea to ammonia  alkalinization of acidic environment 
survival of bacteria in gastric lumen
• Bacterial colonization and attachment to epithelial cells  Release of cytotoxins
(eg. cagA toxin)
• urease, catalase, vacuolating cytotoxin, lipopolysaccharide
• more common in lower socioeconomic group

10. NSAIDs
• NSAIDs inhibit cyclooxygenases (i.e., COX-1 and COX-2)
• Impairs prostaglandin synthesis
• Decrease mucosal blood flow
• Inhibit the release of nitric oxide (NO) and hydrogen sulfide (H2S)
• Enhances neutrophil adherence
• 15-20% incidence with regular use of NSAIDs

11. • Duodenal and pre-pyloric peptic ulcers : Gastric acid level is higher
• Gastric ulceration : Gastric acid level is relatively normal
• Severe physiologic stress
- Cushing ulcers  brain tumor or injury, single, deep ulcers, prone to perforation,
associated with high gastric acid output, stomach
- Curling ulcers  Extensive burns, prone to perforation, 1st part of duodenum
• Gastrinoma (Zollinger-Ellison syndrome) or multiple endocrine neoplasia type I
(MEN-I)
• Smoking: Smokers are about twice as likely to develop PUD as nonsmokers
• Alcohol : No confirmatory data

12. Other risk factors
• Physiologic risk factors
Increase in BAO [OR 3.5]
Increase in MA
no correlation between acid
secretion and the severity of PUD
• Genetics
20% have family history
• Uremic gastropathy
• Cytomegalovirus infection
• Bile gastropathy
• Granulomatous gastritides (eg,
sarcoidosis, histiocytosis X,
tuberculosis)
• 5-fluorouracil (5-FU),
methotrexate (MTX), and
cyclophosphamide
• Use of crack cocaine :
Juxtapyloric, Perforation

13. History
• Sex: Duodenal Ulcer – M:F = 2:1; Gastric Ulcer – M:F=1:1
• Age: Gastric Ulcer Pts are older than Duodenal Ulcer Pts
• Pain
>90% pts with PUD
Mechanism of pain is unclear
Epigastric
May Radiate to back (Bailey & Love, 27th ed); Non radiating (Schwartz, 11th ed)
Duodenal Ulcer : 2-3 hrs after meal and at night (2/3rd : Awaken from sleep)
Gastric Ulcer : Occurs with eating, doesn’t awaken from sleep

14. History
• Abdominal pain is acute, severe and sharp if perforation occurs
• Periodicity
• Nausea
• Bloating
• Hematemesis or melena resulting from gastrointestinal bleeding.
• Weight loss
• Occult blood in stool
• Symptoms suggestive of anemia like fatigue or dyspnea

16. Physical examination
• Unperforated Peptic Ulcer Disease
Epigastric tenderness
Melena
Succussion splash due to gastric outlet obstruction
• Perforated Peptic Ulcer Disease
Fetal position
Generalized tenderness
rebound tenderness
Guarding
Rigidity
Hypotension
Tachycardia
Anuria
Septic Shock

17. Gastric Ulceration : Modified Johnson Classification
Type I: Ulcer along the body of the stomach,
most often along the lesser curve at incisura
angularis.
Type II: Ulcer in the body in combination with
duodenal ulcers.
Type III: In the pyloric channel within 3 cm of
pylorus.
Type IV: Proximal gastroesophageal ulcer.
Type V: Can occur throughout the stomach.
Associated with the chronic use of NSAIDs

18. Differential diagnosis
• Acute Cholecystitis and Biliary Colic
• Acute Coronary Syndrome
• Acute Gastritis
• Esophageal rupture and tears
• Gastroesophageal Reflux Disease
• Inflammatory Bowel Disease
• Gastric Carcinoma
• Nonulcer dyspepsia (NUD) or functional dyspepsia

19. Investigations
• Testing for H. pylori : All patients with active or past history of peptic ulcer disease
(unless previous cure of HPI has been documented). (1)
Rapid Urease Test
Urea breath test
Fecal antigen test
or Biopsy-based testing
The 2017 American College of Gastroenterology (ACG) guidelines for the
treatment of H pylori infection (HPI)

20. Investigations
• Chest Xray to look for perforation

21. Investigations
• Upper gastrointestinal (GI) endoscopy : preferred diagnostic test. ‘Gold standard’
– Bailey & Love
Gastric Ulcers Duodenal Ulcers
Most occur at the junction of the fundus and
antrum, along the lesser curvature
discrete mucosal lesions
punched-out smooth ulcer base
filled with whitish fibrinoid exudate
solitary and well circumscribed
Malignancy relatively more common
>95% in 1st part of duodenum
well-demarcated break in the mucosa
may extend into the muscularis propria
Malignancy uncommon

22. Benign gastric ulcer Malignant gastric ulcer
Mucosal folds
Converging mucosal
folds up to the margin
Effacing mucosal folds
Site 95% lesser curve Greater curvature
Margin Regular margin Irregular margin
Floor Granulation tissue in floor Necrotic slough in floor
Edge
Not everted; punched or
sloping
Everted edge
Surrounding area
Surrounding area and
rugae are normal
Surrounding area shows
nodules, ulcers and
irregularities
Size and extent
Small, deep up to part of
muscle layer
Large and deep

23. Forrest classification

24. Duodenal Ulcer Ia Duodenal Ulcer IIa

25. Duodenal Ulcer IIb Gastric Ulcer IIc

26. Duodenal Ulcer III Gastric Ulcer III

27. Investigations
Ultrasonography
Transabdominal USG is helpful to identify conditions mimicking PUD, like Biliary colic.
Endoscopic ultrasound (EUS) : useful in the evaluation of gastric mass lesions
Barium meal X-ray
- Gastric Ulcer : Niche on lesser curvature, Notch on greater curvature
- Duodenal Ulcer : Absence of duodenal cap, Trifoliate duodenum
CT Scan with oral contrast
- Preferred over Barium meal
- Provides anatomical information like in case of rolling hiatus hernia

28. Arrows: Tumor infiltrating through Serosa
Arrowheads: Enlarged LN

29. Treatment
• Proton Pump Inhibitors (PPI)
- Mainstay of treatment of PUD
- Renders the patient achlorhydric
- All benign ulcers heal, majority within 2 weeks
• H. pylori eradication therapy : Triple Therapy
1. Proton pump inhibitor (PPI)
2. Clarithromycin (500 mg) or metronidazole 500 mg BID (when Clarithromycin
resistance is increasing)
3. Amoxicillin 1000 mg BID or metronidazole 500 mg BID

30. Surgical treatment of duodenal ulcer
Indications
Perforation
Obstruction
Bleeding
Intractability or nonhealing

31. Treatment
Billroth I Billroth II Gastrojejunostomy

32. Truncal Vagotomy Highly Selective Vagotomy

33. Heineke Mikulicz Pyloroplasty

34. Complications
• Bleeding
- by erosion into the left
gastric and rarely splenic
vessels or to vessels in
the wall of ulcer
- Common in type II and III
gastric ulcers
- Surgery
Oversewing of the ulcer
with or without vagotomy
and drainage
Vagotomy + Antrectomy

35. Complications
• Perforated Peptic Ulcer
Most common site is anterior wall of duodenum
Anterior or incisural gastric ulcer may also
perforate
Investigations:
Erect Chest Xray : Gas Under Diaphragm
Serum amylase : Elevated but not diagnostic
CT scan is diagnostic

36. Treatment of Perforated Peptic Ulcer
• Resuscitation
• Analgesia
• Systemic antibiotics
• Surgery

37. Hx : History
Rx : Investigation
HSV : Highly
Selective vagotomy
TV/D : Truncal
Vagotomy &
Drainage
Bx : Biopsy

38. Other Complications
Duodenal Ulcer Gastric Ulcer
Pyloric stenosis Hourglass contracture
Penetration to pancreas Teapot deformity
Malignant transformation (5-10%)

39. Thank you