• PUD are defects in the gastric or duodenal mucosa that extend
through the muscularis mucosa or ulceration of any part of GIT
exposed to gastric juice.
• Is an ulcer in the wall of stomach or duodenum resulting from the
digestive action of the Gastric juice on the mucus membrane when
the latter is rendered susceptible to it’s action.(as from infection with
bacterium Helicobacter pylori or the chronic use of NSAIDs).
• Gastric ulcer
1. Pain occur 1-2hrs after meals.
2. Accentuated by ingestion of food.
3. Risk of malignancy.
4. Deep and penetrating are usually occur on the lesser curvature of the
5. Pain usually does not wake patient.
• Duodenal ulcer
1. Pain occur 2-4hrs after meals
2. Pain wakes up the patient
3. Pain relieved by food
4. Very little risk for malignancy.
6. Risk factors
• Most PUD occur in the presence of acid and pepsin when H pylori,
NSAIDS or other factors disrupt normal mucosal defense and healing
• Being gastric ulcer occur anywhere in the stomach (mostly in lesser
curvature).most duodenal ulcer occur in the first part of duodenum.
• Risk factors for NSAIDS induced ulcer and upper GI complications
1. Age greater than 60, previous peptic ulcer,high dose NSAIDS,choice
of NSAIDS,Aspirin, NSAIDS related dyspepsia,RA,alcohol
• A physical imbalance between aggressive factors (gastric acid and pepsin)and
protective factors (mucosal defense and repair) remain important issue
• Gastric acid is secreted by the parietal cells,which contain receptors for
histamine,gastrin and acetylcholine.
• Increased acid secretions is observed in patients with duodenal ulcer and may be
in H pylori infection.
• Patients with gastric ulcer usually have normal or reduced rate of acid secretions.
• Pepsin is an important cofactor that play a role in the proteolytic activity involved
in ulcer formation.
• Mucosal defense and repair mechanism protect the gastroduodenal mucosa from
noxious endogenous and exogenous substance.
8. • The viscous nature and near neutral pH of mucus bicarbonate barrier protect the
stomach from the acid contents in the gastric lumen.
• Gastric hyperemia an increased prostaglandin synthesis characterize adaptive
cytoprotection,the short term adaptation of mucosal cells to mild topical
• This enables the stomach to initially withstand the damaging effect of irritants.
• Alterations in mucosal defense that are induced by H pylori or NSAIDS are the
most important cofactors in the formation of peptic ulcer.
1. H pylori
• Its structure permits it to move from the lumen of the stomach,where the pH is
low,to the mucus layer,where the local pH is neutral.
• The acute infection is accompanied by transient hypochlorhydria,which permits
the organism to survive in the acidic gastric juice.
• H pylori produces large amount of urease,which hydrolyzes urea in the gastric
juice and converts it to ammonia and carbon dioxide.
9. • The local buffering effect of ammonia creates a neutral micro environment within
and surrounding the bacterium,which protect it from the lethal effect of acid.
• H pylori produces acid inhibitory protein which allow it to adapt the low pH
environment of stomach.
• H pylori attaches to gastric type epithelium which prevent the organism from
being shed during cell turnover and mucus secretions.
• Pathogenic mechanism include :
1. Direct mucosal damage
2. Alternations in the host immune response.
3. Hypergastrinemia leading to increased acid secretions
4. H pylori enhances the carcinogenic conversion of susceptible gastric epithelial
• Including Aspirin cause gastric mucosal damage by two important mechanism
1. Direct or topical irritation of the gastric epithelium
2. Systemic inhibition of endogenous mucosal prostaglandin synthesis.
• COX is the rate limiting enzyme in the conversion of arachidonic acid to
prostaglandin and is inhibited by NSAIDS.
• Eg: Indomethacin, Ibuprofen,Ketorolac,Diclofenac,Valdecoxib, Aspirin.
• Topical irritants properties are predominantly associated with acidic NSAIDS
and their ability to decrease the hydrophobicity of the mucusgel layer in the
• Lab test
1. The hematocrit and hemoglobin are low with bleeding and stool
hematocrit test are positive.
2. Endoscopic test
• Histology using various stains
• Culture of biopsy
• Biopsy urease
3. Non endoscopic test
• Antibody detection
• Urea breath test
• Stool antigen.
• Upper GI bleeding, perforation, obstruction.
• Bleeding caused by erosion of an ulcer in to an artery
• Melena,hematemesis,ulcer related perforation into the peritoneal
cavity, gastric outlet obstruction due to scarring or edema of the
duodenal bulb can leads to gastric retention.
17. Patient education
• Avoid alcohol,coffee, caffeinated soda,fatty foods, chocolate and spicy
• Avoid eating late night snacks.
• Avoid tobacco use because it will slows the healing of ulcer and
increase the risk of recurrence.
• Call Doctor when you feel:
1. Sudden ,sharp abdominal pain,fainting, excessive sweating,vomiting
blood,blood in your stool.
• Text book of pharmacotherapy by Joseph T Dipiro