PEPTIC ULCER DISEASE

Dr Amit Bhattarai
Consultant General &
Laparoscopic surgeon
Focal defects in the gastric or duodenal
mucosa or submucosa or deeper usually
5mm to 1cm
Imbalance between mucosal defenses and
acid peptic injury
Gastritis is the precursor to PUD and is
clinically difficult to differentiate the two
Lifetime prevalence=10% of Americans
develop PUD
10% of the ER patients with abdominal
pain diagnosed with PUD
Prevalence decreasing over last 30 yrs
Male to female ratio of gastritis =1:1
Male to female ratio of PUD= 2:1
Peak age 70yrs
Helicobacter pylori
NSAIDs
Smoking
Acid pepsin vs. mucosal resistance

Diet/other diseases/genetics/emotional
stress

ETIOLOGY
3 level barrier preepithelial, epithelial and
subepithelial elements

Mucus-HCO3 layer serves as a

phycicochemical barrier

Epithelial cells have ionic transporters that

maintain intracellular pH and HCO3
production
Intercellular tight junctions

Gastroduodenal mucosal defense

Slow growing,microaerophilic,motile,gram
–ve,spiral flagellated bacteria
Discovered by Robin Warren and Barry
Marshall
50% of the population infected,a major
cause of chronic gastritis
Transmitted via feco-oral route
Secretes urease; converts urea to
ammonia

Helicobacter pylori
Produces alkaline environment enabling
the survival
Higher prevalence in lower socioeconomic
group
90% of the Du ulcers vs 70% of the
gastric ulcers +ve
Asymptomatic in approx.70% infected
Considered class I carcinogen---- gastric
Ca;gastric lymphoma
NATURAL HISTORY OF H PYLORI
Prostaglandins
-abundant in gastric mucosa
-play central role in epithelial
defense/repair
-regulate release of mucosal HCO3 and
mucus
-inhibit parietal cell secretion
-maintain mucosal blood flow
-epithelial cell restitution
 4 times as common as gastric ulcers
Most common in the middle age (30-50 y)
Male to female ratio---5:1
Genetic link: 3 times common in 1st
degree
Blood group O
Increased serum pepsinogen
H pylori---upto 95%
Smoking twice as common

Duodenal ulcers
Common in late middle age(incidence
increases with age)
Male to female ratio---2:1
More common in blood group A
Use of NSAIDs– 3-4 times increased risk
H pylori---70%
10-20% harbouring concomitant Du ulcer

Gastric ulcers
Interplay between host and
bacterial factors
 Causative in 30 % GU, less of DU
 Interference with PG E levels –impaired
cyto protection
 Increased risk of complications

NSAIDS
Increases Hcl output
Decreases PG levels
Decreases duodenopancreatic HCO3 levels
Increases duodenogastric reflux

Increased risk of GU than DU

Smoking
Curling ulcers: duodenal ulcers and /or
duodenitis in burn patients
Cushing’s ulcer: acute peptic ulceration in
patients with head injury
Stressful life events??
Use of crack cocaine: juxtapyloric ulcers
with propensity to perforate
Alcohol???

Stress and others

 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.
 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.
 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
 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
 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
 Diagnostic Evaluation

► Poor predictive value of abdominal

pain for the presence of a
gastroduodenal ulcer
► Multiple disease that can mimic this
disease
► Empirical therapy is appropriate for
pts who are otherwise healthy and
<45, before embarking on a
diagnostic evaluation .
Sensitivity for detecting a DU
◦ Single contrast—80%
◦ Double contrast—90%

Sensitivity decreased in:

- small ulcers(<0.5cm)
-presence of previous scarring
-postop period

Barium studies
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.

Endoscopy
 Test Sensitivity Comments
/
Tests for Detection of H. pylori
Specificity
,%
Invasive (Endoscopy/Biopsy Required) 
Rapid urease 80– Simple, false negative with recent use
95/95– of PPIs, antibiotics, or bismuth
100 compounds
Histology 80–90/ provides histologic information
>95
Culture —/— Time-consuming, expensive ; antibiotic
susceptibility
Non-invasive 
Serology >80/>90 Inexpensive, convenient; not useful for
early follow-up
Urea breath >90/>90 Simple, rapid; useful for early follow-
test up; false negatives with recent
therapy ; exposure to low-dose
radiation with 14C test
 
 Management
► General measures
 Stop smoking

 Avoid NSAIDs and alcohol

 Dietary modifications?

 Treat/avoid stress
 Peptic Ulcer Disease: Treatment
Drug Type/Mechanism Examples Dose
Acid-suppressing drugs    
  Antacids
  H2 receptor antagonists Ranitidine 300 mg hs
  Famotidine 40 mg hs
Nizatidine 300 mg hs
  Proton pump inhibitors Omeprazole 20 mg/d
Lansoprazole 30 mg/d
Rabeprazole 20 mg/d
Pantoprazole 40 mg/d
Esomeprazole 20 mg/d
Mucosal protective agents    
  Sucralfate Sucralfate 1 g qid
  Prostaglandin analogue Misoprostol 200 g qid
  Bismuth-containing Bismuth subsalicylate
compounds (BSS)
 Regimens for H. pylori
eradication
Drug Dose
Triple Therapy 
1. Bismuth subsalicylate plus  2 tablets qid
  Metronidazole plus  250 mg qid
  Tetracyclinea  500 mg qid
2. Ranitidine bismuth citrate 400 mg bid
plus 
  Tetracycline plus  500 mg bid
  Clarithromycin or 500 mg bid
metronidazole
3. Omeprazole (lansoprazole) 20 mg bid (30 mg bid)
plus 
  Clarithromycin plus  250 or 500 mg bid
  Metronidazoleb or  500 mg bid
 
 Regimens for H. pylori
eradication
Quadruple Therapy 

Omeprazole (lansoprazole) 20 mg (30 mg) daily

Bismuth subsalicylate 2 tablets qid

Metronidazole 250 mg qid

Tetracycline 500 mg qid

Highlyselective vagotomy
Truncal vagotomy with pyloroplasty
Truncal vagotomy with antrectomy

Surgical management
Gastrointestinal bleeding:15%
Perforation/peritonitis: 7%
Gastric outlet obstruction: 1-2%
Gastric carcinoma

PUD Related Complications

Also called parietal cell vagotomy or
proximal gastric vagotomy
Severs the proximal 2/3rd vagal supply
Gastric acid secretion reduced by 75%
Though less side effects ,supplanted by
long term PPI
Low mortality(<0.5%),high
recurrence(10%)

Highly selective vagotomy

Truncal vagotomy and pyloroplasty,and
truncal vagotomy and G-J
Easy and quicker to perform
Significant dumping and/diarrhea in 10%
Oesophageal perforation;lethal
complication
Useful in complicated ulcers esp. II and
III
Gastric ulcer to be excised or biopsied

Vagotomy and drainage

procedures
Heineke-Mikulicz type (most common)
Finney type
Jaboulay type

pyloroplasties
Low ulcer recurrence rate(<0.2%)
Useful for complicated ulcers
High operative mortality rate(1%)
Reconstruction with Billroth I or Billroth II
loop G-J
Avoided in hemodynamically unstable
patient,extensive inflammation and
scarring of the proximal duodenum

Truncal vagotomy and antrectomy

Indications Doudenal Gastric

Oversew Oversew and biopsy

Bleeding Oversew,V+D Oversew,biopsy and
V+A V+D
Distal gastrectomy
Patch Biopsy and patch
Perforation Patch,HSV Wedge excision,V+D
Patch,V+D Distal gastrectomy

HSV+GJ Biopsy,HSV+GJ
Obstruction V+A Distal gastrectomy

Surgical options for complications

Intractibility/ HSV HSV and wedge
Nonhealing V+D excision
V+A Distal gastrectomy
Thank u