Peptic Ulcer Disease

 What is Peptic Ulcer Disease (PUD)

 Epidemiology

◦ Gastric Ulcers
◦ Duodenal Ulcers
 Agents
 Etiology
 Clinical Manifestation of PUD
 Diagnostic Plan
 Images

◦ Endoscopy
 A chronic disease with multiple complaints
(dyspeptic syndrome) located in stomach
(gastric ulcer) and or duodenum (duodenal
ulcer), characterised by an circumscribed
ulcerous crater which penetrates the
muscularis mucosa.
 Higher prevalence in developing countries.
◦ DU 8-10% and annual incidence of 0,2%
◦ GU 3 times more rare
◦ Decrease in incidence since 1970
◦ Decrease of DU principally in men M/F 3-4/1, 2/1
and even 1/1
◦ GU no significant modifications in incidence.
◦ Decreased incidence principally in young and
middle aged men; is becoming a disease of old
age.
 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 80%
 10 - 20% of patients with a gastric ulcer have
a concomitant duodenal ulcer
 Duodenal sites are 4x as common as gastric
sites
 Most common in middle age
◦ peak 30-50 years
 Male to female ratio—4:1
 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
 Helicobacter Pylori + ulcer
 NSAID (aspirin) induced ulcer
 Stress induced ulcer
 Ulcer which accompanies genetic diseases
and syndromes
 Helicobacter negative ulcer.
 Smoking
 Ethanol
 Bile acids
 Steroids
 A peptic ulcer is a mucosal break, 3 mm or greater, that
can involve the stomach or duodenum.
 The most important contributing factors are H pylori,
NSAIDs, acid, and pepsin.
 The most important aggressive factors implicated in ulcer
◦ Acid hypersecretion
Increase in parietal cell mass
Increase in vagus tone
Increase in parietal cellular sensibility to gastrin
Antral G cells hyper function
Nocturnal acid hypersecretion
Deterioration in inhibitory mechanism of acid secretions
Motility disturbances: Duodenal ulcer-rapid gastric emptying, gastric
ulcer- gastric hypomotility
◦ Pepsin hypersecretion
Hiperpepsinogenemia I
-Helicobacter pylori
◦ Duodenogastric reflux
Biliary acids, lisolecitin and proteolytic enzymes.
 Factors of defence
◦ Pre-epithelial factors
Bicarbonate and mucus barriers
Tensioactive phospholipids
◦ Epithelial factors
Cellular resistance (normal cellular metabolism)
Intra-cellular PH maintenance
Growth factors (epithelial growth factors,
Prostaglandins, NO)
Mechanism of repair of epithelial lesions
◦ Post-epithelial factors
Abnormal mucous blood flow
 Individual factors
◦ Genetic factors: group 0 & A, Lewis and non-
secretory factor (a-b-)
◦ Familial Hyperpepsinogenemia type I
◦ Studies: 39% genetic factors and 61% average
predisposing factors
◦ Associated diseases : ZE syndrome, MEN I,
systemic mastocytosis, alfa 1 antitrypsin
deficiency, hepatic cirrhosis, chronic pancreatitis,
Crohn’s disease, COPD, polycythemia vera,
basophilic leukemia, amyloidosis
◦ Personality changes : anxiety, neuralgia
 80-90% of ulcers after excluding AINS
 Increased risk 4x duodenal ulcer and 3x gastric
ulcer
 Decreased risk of recurrence if eradication is
successful: 6% 1 yr and 17% > 1 yr, superior
supraselective vagotomy.
 Reversible gastrine hypersecretion
predominant postprandial
 Increase in acid secretion if gastritis is antral
 Hipersecretion of pepsinogen
 Changes in adherent mucus
 Changes in appearance of gastroduodenal
mucus.
 Mucus, bicarbonate secretion, microcirculation
(mucosal appearance depends upon PG (PGE)
 NSAIDS inhibits COX1 and COX2 by decreasing
physiological and pathological prostaglandins
(systemic effect )
 Some of NSAID (weak acids) have mucosal
irritant effect (local effect )
 NSAID and HP are independent factors in
ulcerogenesis but have additional effects (to
eradicate HP before starting treatment with
NSAID)
 Mucosal adaptation
 Zollinger Ellison Syndrome (gastrinoma)
isolated or in association with MEN I (0,5%)

Stress Ulcer
 Acid hypersecretion
 Systemic arterial hypotension
 Stress coagulopathy
 Ischemic induced mucosal defects.
 Signs and symptoms

Early Vomitin Pancreati Bleedin Peritoni

Nausea tis(Perfor
Satiety g tis g
ation)
Abdominal
Epigastric
Pain

PEPTIC
ULCER
 Stool for fecal occult blood
 Labs: CBC, liver function test, amylase, and
lipase.
 H. Pylori can be diagnosed by urea breath test,
blood test, stool antigen assays, & rapid urease
test on a biopsy sample.
 Upper GI Endoscopy: Any pt >50 yo with new
onset of symptoms or those with alarm
markings including anemia, weight loss, or GI
bleeding.
◦ Preferred diagnostic test b/c its highly sensitive for dx
of ulcers and allows for biopsy to rule out malignancy
and rapid urease tests for testing for H. Pylori.
Endoscopy
Endoscopy
Endoscopy
Typical radiographic features of benign gastric ulcer (a)
Typical radiographic features of benign gastric ulcer (c)
Typical radiographic features of benign gastric ulcer (d)
Typical radiographic features of benign gastric ulcer (e)
Benign gastric ulcer (b)
Typical radiographic features of duodenal ulcer (b)
Typical radiographic features of duodenal ulcer (c)
Duodenal ulcer (a)
Duodenal ulcer (b)
 Acute:
◦ bleeding (hematemesis, melena)
◦ perforations
 Chronic:
◦ pyloric stenosis
◦ cancer
 Perforation & Penetration—into pancreas,
liver and retroperitoneal space
 Peritonitis
 Bowel obstruction, Gastric outflow obstruction
 Bleeding--occurs in 25% to 33% of cases and
accounts for 25% of ulcer deaths.
Stigmata of recent hemorrhage (a)
Stigmata of recent hemorrhage (b)
Stigmata of recent hemorrhage (c)
Stigmata of recent hemorrhage (d)
Stigmata of recent hemorrhage (e)
Stigmata of recent hemorrhage (f)
Stigmata of recent hemorrhage (g)
Stigmata of recent hemorrhage (h)
Perforated peptic ulcer
Pyloric outlet obstruction and peripyloric ulcer disease (b)
Pyloric outlet obstruction and peripyloric ulcer disease (c)
Pyloric outlet obstruction and peripyloric ulcer disease (d)
Pyloric Stenosis – Paraclinic
Investigation