PATHOPHYSIOLOGY OF ULCER

1. ULCERSULCERS
BYBY
IBEKWE CHIGOZIE BLESSINGIBEKWE CHIGOZIE BLESSING

2. Ulcer diseaseUlcer disease
 ulcer is a defect of gastric or duodenal mucosa whichulcer is a defect of gastric or duodenal mucosa which
interfere over lamina muscularis mucosae, submucosa orinterfere over lamina muscularis mucosae, submucosa or
penetrates across whole gastric or duodenal wallpenetrates across whole gastric or duodenal wall
 rise of ulcer is conditioned by presence of acid gastricrise of ulcer is conditioned by presence of acid gastric
contentcontent
 frequent disease, men are afected 3-4x more than womenfrequent disease, men are afected 3-4x more than women

3.  Classification:Classification:
Acute ulcer (ulcus acutum)Acute ulcer (ulcus acutum)
 smooth non-elevated borders and smooth basesmooth non-elevated borders and smooth base
 major bleeding into upper GITmajor bleeding into upper GIT
Chronic ulcer (ulcus chronicum)Chronic ulcer (ulcus chronicum)
 rushed and elevated boders, inflammation withrushed and elevated boders, inflammation with
hypertrophic and fibrotic proliferation is presenthypertrophic and fibrotic proliferation is present
 tthe most frequent form of ulcer diseasehe most frequent form of ulcer disease
• Ulcus chronicum mediogastricumUlcus chronicum mediogastricum
• Ulcus chronicum ventriculi et duodeniUlcus chronicum ventriculi et duodeni
• Ulcus chronicum praepyloricumUlcus chronicum praepyloricum
• Ulcus chronicum duodeniUlcus chronicum duodeni

4. Comparing duodenal and gastricComparing duodenal and gastric
ulcersulcers

5. Gastric ulcersGastric ulcers
 common in late middle agecommon in late middle age
 incidence increases with ageincidence increases with age
 Male to female ratio—2:1Male to female ratio—2:1
 More common in patients with blood group AMore common in patients with blood group A
 Use of NSAIDs - associated with a three- to four-foldUse of NSAIDs - associated with a three- to four-fold
increase in risk of gastric ulcerincrease in risk of gastric ulcer
 Less related to H. pylori than duodenal ulcers – about 80%Less related to H. pylori than duodenal ulcers – about 80%
 10 - 20% of patients with a gastric ulcer have a concomitant10 - 20% of patients with a gastric ulcer have a concomitant
duodenal ulcerduodenal ulcer

6.  SymptomsSymptoms of gastric ulcer diseaseof gastric ulcer disease::
 eepigastric pain after meal or during mealpigastric pain after meal or during meal
 uupper dyspeptic syndrome – loss of appetite, nauzea,pper dyspeptic syndrome – loss of appetite, nauzea,
vomiting, flatulencevomiting, flatulence
 vvomiting brings reliefomiting brings relief
 rreduced nutritioneduced nutrition
 lloss of weightoss of weight

7. Duodenal UlcersDuodenal Ulcers
 duodenal sites are 4x as common as gastric sitesduodenal sites are 4x as common as gastric sites
 most common in middle agemost common in middle age
 peak 30-50 yearspeak 30-50 years
 Male to female ratio—4:1Male to female ratio—4:1
 Genetic link: 3x more common in 1Genetic link: 3x more common in 1stst
degree relativesdegree relatives
 more common in patients with blood group Omore common in patients with blood group O
 associated with increased serum pepsinogenassociated with increased serum pepsinogen
 H. pylori infection commonH. pylori infection common
 up to 95%up to 95%
 smoking is twice as commonsmoking is twice as common

8.  Symptoms of duodenal ulcer disease:Symptoms of duodenal ulcer disease:
 epigastric pain 2 hours after meal or on a emptyepigastric pain 2 hours after meal or on a empty
stomach or during nightstomach or during night
 pyrosispyrosis
 good nutritiongood nutrition
 obstipationobstipation
 seasonal dependence (spring, autumn)seasonal dependence (spring, autumn)

9. Gastric ulcerGastric ulcer Duodenal ulcerDuodenal ulcer

10. EtiologyEtiology
 A peptic ulcer is a mucosal break, 3 mm or greater, that canA peptic ulcer is a mucosal break, 3 mm or greater, that can
involve the stomach or duodenum.involve the stomach or duodenum.
 The most importantThe most important contributing factorscontributing factors areare H pylori,H pylori,
NSAIDs, acid, and pepsin.NSAIDs, acid, and pepsin.
 AdditionalAdditional aggressive factorsaggressive factors include smoking, ethanol, bileinclude smoking, ethanol, bile
acids, aspirin, steroids, and stress.acids, aspirin, steroids, and stress.
 ImportantImportant protective factorsprotective factors are mucus, bicarbonate,are mucus, bicarbonate,
mucosal blood flow, prostaglandins, hydrophobic layer, andmucosal blood flow, prostaglandins, hydrophobic layer, and
epithelial renewal.epithelial renewal.
 Increased risk when older than 50 d/t decrease protectionIncreased risk when older than 50 d/t decrease protection
 When an imbalance occurs, PUD might develop.When an imbalance occurs, PUD might develop.

11. Role ofRole of H. Pylori infection in theH. Pylori infection in the
pathogenesis of peptic ulcer:pathogenesis of peptic ulcer:
 H. pylori infection is present in almost allH. pylori infection is present in almost all
patients with duodenal ulcers and 70% casespatients with duodenal ulcers and 70% cases
with gastric ulcers.with gastric ulcers.
 Duodenal ulcers - Usually associated withDuodenal ulcers - Usually associated with
gastritis confined to the antrum.gastritis confined to the antrum.
 Gastric ulcers - Usually associated withGastric ulcers - Usually associated with
pangastritis.pangastritis.

12. Mechanism:Mechanism:
H. pylori secretes urease (generatesH. pylori secretes urease (generates
ammonia), protease (breaks downammonia), protease (breaks down
glycoprotein in the gastric mucus) orglycoprotein in the gastric mucus) or
phospholipases.phospholipases.
Bacterial lipopolysaccharide attractsBacterial lipopolysaccharide attracts
inflammmatory cells to the mucosa.inflammmatory cells to the mucosa.
Neutrophils release myeloperoxide.Neutrophils release myeloperoxide.

13.  A bacterial platelet-activating factorA bacterial platelet-activating factor
promotes thrombotic occlusion of surfacepromotes thrombotic occlusion of surface
capillaries.capillaries.
 Mucosal damage allows leakage of tissueMucosal damage allows leakage of tissue
nutrients in the surface microenvironment ,nutrients in the surface microenvironment ,
sustaining the bacillussustaining the bacillus
 Damage of the protective mucosal layer.Damage of the protective mucosal layer.
The epithelial cells are exposed to theThe epithelial cells are exposed to the
damaging effect of acid-peptic digestion.damaging effect of acid-peptic digestion.
 Inflammation of the gastric mucosa.Inflammation of the gastric mucosa.
 Chronically inflamed mucosa moreChronically inflamed mucosa more
susceptible to acid- peptic injury and pronesusceptible to acid- peptic injury and prone
to peptic ulcerationto peptic ulceration

14.  Ulcers occur at sites of chronicUlcers occur at sites of chronic
inflammation .inflammation .
Eg - AntrumEg - Antrum
- Junction of antral and body- fundic- Junction of antral and body- fundic
mucosa (division between the inflamedmucosa (division between the inflamed
antral mucosa and normal acid secretingantral mucosa and normal acid secreting
mucosa).mucosa).
 Pangastritis - When there is extensivePangastritis - When there is extensive
gastritis, the ulcers are more proximallygastritis, the ulcers are more proximally
situated. In elderly patients gastric ulcers aresituated. In elderly patients gastric ulcers are
more proximally situated as there ismore proximally situated as there is
proximal migration of the antral-bodyproximal migration of the antral-body
mucosal junctionmucosal junction

15. Other factors causing ulcerOther factors causing ulcer
 Peptic ulcer caused due toPeptic ulcer caused due to high gastrin levelhigh gastrin level
and excess acidand excess acid productionproduction. Gastrinoma. Gastrinoma
may cause multiple peptic ulceration as inmay cause multiple peptic ulceration as in
Zollinger Ellison syndrome. There isZollinger Ellison syndrome. There is
increased parietal cell mass.increased parietal cell mass.
 Peptic ulcers caused due toPeptic ulcers caused due to impairedimpaired
mucosal defensemucosal defense . The. The gastric acid andgastric acid and
pepsin levels are normalpepsin levels are normal andand no H.pylorino H.pylori areare
present.present.

16.  Chronic use of NSAIDs (aspirin) causesChronic use of NSAIDs (aspirin) causes
suppression of mucosal prostaglandin andsuppression of mucosal prostaglandin and
direct irritative topical effect.direct irritative topical effect.
 Repeated use of corticosteroid in high dose.Repeated use of corticosteroid in high dose.
 Cigarette smoking impair healing andCigarette smoking impair healing and
favour recurrences.favour recurrences.
 Alcoholic cirrhosis.Alcoholic cirrhosis.
 Personality, psychological stress, ischemia.Personality, psychological stress, ischemia.


17.  Pathogenesis:Pathogenesis:
 mmultifactorialultifactorial
 ddysbalance between protective andysbalance between protective and aaggressive factorsggressive factors
- Protective f.:Protective f.: saliva, food, alcalic duodenal fluid,saliva, food, alcalic duodenal fluid, mmucus -ucus -
mucine, fast regeneration of gastric epithelial cells, wellmucine, fast regeneration of gastric epithelial cells, well
perfused gastric mucosaperfused gastric mucosa
- Aggressive f.:Aggressive f.: HCl, pepsin, bile acids (reflux), helicobacterHCl, pepsin, bile acids (reflux), helicobacter
pylori, drugspylori, drugs (analgetics(analgetics,, aspirin, korticoids),aspirin, korticoids), nicotine,nicotine,
alcoholalcohol

18.  Complications:Complications:
 BleedingBleeding - chronic (minor, cause anaemia)- chronic (minor, cause anaemia)
- acute (major, form affected vessel)- acute (major, form affected vessel)
 PerforationPerforation - mostly bulbus duodeni, anterior gastric- mostly bulbus duodeni, anterior gastric wallwall
- acute violent pain- acute violent pain
- bleeding can be present- bleeding can be present
 PenetrationPenetration -- of the ulcer deeply through whole wall intoof the ulcer deeply through whole wall into
neighbor organneighbor organ (pancreas, liver)(pancreas, liver)
 StenosisStenosis - narrow of- narrow of thethe lumenlumen causedcaused byby scar,scar, oedema oroedema or
inflammatory infiltration after healing of the ulcerinflammatory infiltration after healing of the ulcer
-- rise only at pyloric localizationrise only at pyloric localization
-- vomiting of huge volume of gastric contentvomiting of huge volume of gastric content

19. Zeman, M. et al., Speciální chirurgie, ISBN 80-7262-260-9, 2004
A – penetration B – perforation
C – bleeding D - stenosis

20.  Therapy:Therapy:
 ConservativeConservative
• regular lifestyleregular lifestyle
• prohibition of the smoking and alcoholprohibition of the smoking and alcohol
• ddiet (proteins, milk and milky products)iet (proteins, milk and milky products)
• pharmacology (antagonistspharmacology (antagonists ofof H2 receptors, antacids,H2 receptors, antacids,
anticholinergicsanticholinergics
 SurgicalSurgical
• BI, BIIBI, BII resectionresection
• proximal selective vagotomyproximal selective vagotomy
• vagotomy with pyloroplasticvagotomy with pyloroplastic
• suture ofsuture of perforatedperforated or haemorrhagic ulceror haemorrhagic ulcer

21. Than you for your attention!!!Than you for your attention!!!