PEPTIC ULCER
DISEASE
Aman Sulehri
Gastric Physiology
Gastroduodenal Mucosal Defense:The mucosal defense system can be divided as a threelevel barrier
1. Preepithelial
2. Epithelial
3. Subepithelial
Definition:“An
ulcer is defined as disruption of the
mucosal integrity of the stomach and/or
duodenum leading to a local defect or
excavation due to active inflammation.”
Types of Peptic Ulcer
I. Depending on the site:
A. Duodenal Ulcer: Typically occurs in the first inch of 1st part of
the duodenum
B. Gastric Ulcer: Occurs in the lesser curvature adjacent to acid
secreting parietal cell mass.
C. Combined: Gastric ulcer type II
Zollinger Ellison syndrome
D. Anastomotic ulcer
II. Depending on the duration:
A. Chronic peptic ulcer
B. Acute peptic ulcer
Epidemiology
• In US, approx 4 million people have PU and 350,000 new cases
are diagnosed each year.
• Around 180,000 patients are hospitalized yearly. And about
5000 people die each year as result of PUD.
• The lifetime likelihood of developing PU is abt 10% for
amercian males and 4% for females.
• The male-to-female ratio for DU is ant 3:1, and for gastric
ulcer abt 1.5 to 2:1.
• DU more common between ages 30-50 years old and GU
more common in people over age 60 years old
Etiology
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Helicobacter pylori infection(90%)
Drugs - anti-inflammatory(NSAIDs) & Corticosteroids
Hyperacidity - e.g.. Zollinger Ellison syndrome.
Food habits(Spicy food, diet poor in vitamins, smoking and
alcohol)
• Diabetes may increase your risk of having H. pylori
• Lifestyle factors, including chronic stress, coffee drinking, may
make more susceptible to damage from NSAIDs or H. pylori if
one is a carrier of this organism. But these factors do not
cause an ulcer on their own.
• Diseases associated with an increased risk of PUD include
cirrhosis, chronic obstructive pulmonary disease, renal failure,
and organ transplantation.
Pathogenesis
H. pylori and Acid Peptic Disorders:
• The bacterium is a gram-negative microaerophilic rod found most
commonly in the deeper portions of the mucous gel coating the
gastric mucosa or between the mucous layer and the gastric
epithelium. It may attach to gastric epithelium but under normal
circumstances does not appear to invade cells.
• It induces an intense inflammatory & immune response. There is
increased production of pro-inflammatory cytokines such as IL-1, IL6 TNF, IL-8. This cytokine is produced by mucosal epithelial cells, and
it recruits and activates neutrophils
• Several bacterial genes products are involved in causing epithelial
cell injury and induction of inflammation.
• H.pylori secrets urease that breaks down urea to form toxic
compounds such as ammonium chloride and monochloramine
• The organism also elaborate phospholipases that damage
surface epithelial cells.
• Bacterial proteases and phospholipases break down the
glycoprotein-lipid complexes in gastric mucus, thus weakening
1st line mucosal defense
• It also enhances gastric acid secretion and impairs duodenal
bicarbonate production thus reducing pH in duodenum
• Several H.pylori are immunogenic, and they cause activation
of both T cells and B cells
• Thromboembolic occlusion of surface capillaries is promoted
by bacterial platelet-activating factor.
• A specific region of the bacterial genome, the pathogenicity
island, encodes the virulence factors cytotoxin-associated
antigen(Cag A) associated with more severe epithelial
damage, greater acute and chronic inflammation, higher
likelihood of PU and gastric cancer
• One important genes regulated by CagA is vacuolating
toxin(VacA) which causes cell injury in vitro and gastric tissue
demage.it also act as urea transporter and hence increasing
permeability of epithelium to urea
NSAIDs associated PU:
Chronic use of NSAIDs suppresses mucosal prostaglandin synthesis by
blocking COX-1 and COX-2
Zollinger-Ellison syndrome associated PU:
Excess gastrin secretion by tumor and hence excess gastric acid
production
• Cigarette smoking impairs mucosal blood flow and healing.
• Corticosteroids in high dose and with repeated use promote ulcer
formation
• Too-rapid gastric emptying, exposing duodenal mucosa to an
excessive acid load
Clinical Features
• Epigastric pain (the most common symptom)
it is said that gastric ulcers present with pain associated or closely
followed by eating ,where-as duodenal ulcer pain is relieved by food.
Burning in nature
Patient awakens with pain at night.
May radiate to the back (consider penetration)
• Increased salivation(water brash)
• Nausea
• Vomiting, which might be related to partial or complete gastric outlet
obstruction
• Dyspepsia, including belching, bloating, distention, and fatty food
intolerance
• Chest discomfort
• Anorexia, weight loss
• Hematemesis(this can occur due to bleeding directly from a gastric
ulcer, or from damage to the esophagus from severe vomiting)
• Melena
Complications
• Gastrointestinal bleeding
• Perforation
• Penetration is when the ulcer continues
into adjacent organs such as the liver and
pancreas.
• Scarring and swelling due to ulcers causes
narrowing in the duodenum and gastric
outlet obstruction
Diagnosis
• Oesophagogastroduodenoscopy(OGD):
Ulcer appears as a crater with/without slough or bleeding .
In GU, routine biopsy is advised to r/o malignancy while in DU biopsy is
done in recurrent cases to r/o H.pylori
• Barium meal study:
DU: Deformed duodenal cap. Trifoliate deformity is seen when
secondary duodenal diverticulum occurs
GU: appears as niche in lesser curvature due to ulcer crater and as
notch on greater curvature due to spasm of stomach
Duodenal Ulcer Gastric Ulcer
DU
GU
Tests for Detection of H. pylori
Invasive (Endoscopy/Biopsy Required);
• Rapid urease test: Simple; sensitivity and specificity of 90 to 99%
Three kits (ie, CLOtest, Hp-fast, Pyloritek) are commercially available,
each containing a combination of a urea substrate and a pH sensitive
indicator. One or more gastric biopsy specimens are placed in the rapid
urease test kit. If H pylori is present, bacterial urease converts urea to
ammonia, which changes pH and produces a color change.
• Histologic test: To directly ascertain presence of H. pylori
• Culture: Allows determination of antibiotic susceptibility
Non-invasive:
• Antibodies: IgG to H pylori can be measured in serum, plasma, or whole
blood.
• Urea breath test: Simple; sensitivity and specificity of 90 to 99%
• Stool antigen: >90 sensitivity, convenient; not established for
eradication but promising
D/D
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Gastritis
Stomach cancer
Gastro esophageal reflux disease
Pancreatitis
Cholecystitis
Inferior myocardial infarction
Referred pain (pleurisy, pericarditis)
Medical Treatment
Surgical Treatment
Indication:
• Intractable pain in spite of treatment with H2 receptor blockers,
omeprazole and not responding to anti H.pylori regime
• Frequent relapses, H.pylori –ve
• Complications of DU:
Gastric outlet obs.
Hemorrhage
Highly Selective Vagotomy(HSV)
• Also called parietal cell vagotomy or proximal gastric
vagotomy and it causes minimal side effects
• In this operation, vagi are not divided at the trunk. Both ant. &
post. Vagus are identified, isolated & preserved. Their
branches (i.e. ant & post greater gastric nerves of latarjet)
which run along the lesser curvature are isolated.
• The branches supplying parietal cell mass are divided, hence it
is called parietal cell vagotomy.
• The terminal fibers of nerve of Latarjet which supply pylorus
are preserved
Vagotomy and Drainage
• Ant & post trunks of vagus are divided just below diaphragm
followed by drainage procedure like gastro-jejunostomy(GJ)
• Vagus is secretomotor to stomach & after vagotomy the
motility of stomach is lost ang gastric stasis occurs, hence
drainage is done
• Post GJ is preferred because it gives a dependent drainage by
food contents due to gravity,
• Alternative pyloroplasty is preferred by few surgeons instead
of GJ in which pylorus is incised longitudinally & sutured
vertically. Thus, the pyloric ring become incompetent and
wide open
Truncal vagotomy
Anterocolic GJ
Retrocolic GJ
Billroth I partial gastrectomy
• Partial gastrectomy is done including
removal of ulcer followed by
gastroduodenal anastomosis
• It has least recurrence rate of less
than 1% but mortality rate is around
1-2%
Billroth II gastrectomy
• It is indicated when gastric ulcer is
located on lesser curvature.
• Here gasterctomy is done below the
ulcer and remnant of stomach is
anastomosed to jejunal loop(gastrojejunal anastomosis)
Thank GOD it finished 