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PEPTIC ULCER DISEASE
Pukar K.C
Kathmandu University School of Medical Sciences
Normal
Esophagus & Stomach
DEFINITIONS
ï‚¢ Ulcer
Breach in the mucosa of the GI tract that extends through
the muscularis mucosa into submucosa or deeper
ï‚¢ Erosion
Epithelial disruption without breach of the muscularis
mucosa
ï‚¢ Peptic Ulcer disease
Circumscribed ulcer that occurs in any part of the GI tract
due to the aggressive action of acid and peptic juices.
SITES OF ULCERS
ï‚¢ First part of
Duodenum
ï‚¢ Lesser curve of
stomach
ï‚¢ Stoma following
gastric surgery
ï‚¢ Oesophagus
ï‚¢ Gastric mucosa within
Meckel’s Diverticulum
ETIOLOGY
ï‚¢ Helicobacter pylori infection
ï‚¢ Chronic NSAIDs and Corticosteroids use
ï‚¢ Cigarette smoking
ï‚¢ Alcohol consumption
ï‚¢ Zolinger-Ellison syndrome
ï‚¢ Hyperparathyroidism and chronic renal failure
PATHOGENESIS
ï‚¢ Zollinger- Ellison syndrome
ï‚— Uncontrolled secretion of gastrin by tumor resulting
massive acid production
ï‚¢ NSAIDs use
ï‚— Direct chemical irritation
ï‚— Suppressing prostaglandin synthesis
ï‚¢ Cigarette smoking
ï‚— Impaired mucosal blood flow and healing
ï‚¢ Hyperthyroidism and chronic renal failure
ï‚— Hypercalcemia induced excessive gastrin secretion
H. PYLORI
ï‚¢ Flagella
ï‚¢ Urease
ï‚— Generates ammonia from endogenous urea and
elevates pH
ï‚¢ Adhesins
ï‚— Enhance bacterial adherance to surface cells
ï‚¢ Toxins
ï‚— CagA gene
H. PYLORI
ETIOLOGIC FACTORS OF PUD
Features Gastric ulcers Duodenal ulcers
Incidence Less common More common
Common Location Antrum, lesser cuvature Anterior wall*, 1st part
Age group Middle age Middle or old age
Male: Female ratio 1:1 4:1
Association with H.
Pylori
65% 85%-100%
Level of gastric acid
secretion
Mostly normal Mostly increased
Malignancy Common Rare
*Kissing ulcers: Both anterior and posterior wall ulcer of
duodenum
TYPES OF GASTRIC ULCER
DAINTREE JOHNSON
•Type I
In the antrum, near lesser
curvature
Normal acid level
•Type II
Combined gastric and
duodenal ulcer
High acid level
•Type III
Prepyloric
High acid level
•Type IV
Ulcer in the proximal
stomach and Cardia
Normal acid level
55% 25%
15% 5%
FEW MORE ULCERS!!!
ï‚¢ Stress ulcer
ï‚— In association with shock, sepsis or severe trauma
ï‚¢ Curling ulcer
ï‚— In association with severe burns or trauma
 Cushing’s ulcer
ï‚— In patients with intracranial disease oor after
neurosurgery
CLINICAL PRESENTATION
ï‚¢ Symptoms
ï‚— Pain
ï‚¢ Epigastric region, burning or aching type
ï‚¢ May radiate to back
ï‚— Heartburn, Nausea, vomiting, bloating, belching, water-
brash
ï‚— Alteration in weight
 Haematemesis or Maelena  presents as anemia
ï‚— Periodicity of symptoms
ï‚¢ Significant past history
ï‚¢ Clinical examination
ï‚— Tender epigastrium
ï‚— Features of complication, if present
Gastric Ulcer Duodenal Ulcer
Pain increased after food intake Pain relieved after food intake
Periodicity less common Periodicity more common
Haematemesis more common Melaena more common
Weight loss common Weight gain occurs
Equal in both sexes More in males
INVESTIGATIONS
ï‚¢ Esophagogastrodeodenoscopy (EGD)
ï‚¢ Barium swallow
ï‚¢ Urea Breath Testing
ESOPHAGOGASTRODEODENOSCOPY
It is fundamental that any gastric ulcer
should be regarded as being
Malignant, no matter how classically it
resemble a benign gastric ulcer
Multiple biopsies should be taken, as many
as 10 well targeted biopsies
ESOPHAGOGASTRODEODENOSCOPY
ï‚— Endoscopic procedure
ï‚— Visualizes ulcer crater
ï‚— Ability to take tissue biopsy to R/O cancer and
diagnose H. pylori
BENIGN GASTRIC ULCER
MUCOSAL
FOLDS
Converging folds
Margin Regular
Floor Granulation tissue in
floor
Edges NOT everted ,punched
Surrounding
Area
Normal
Size and
Extent
Small deep up to
muscle layer
MALIGNANT GASTRIC ULCER
MUCOSAL
FOLDS
Effacing Mucosal folds
Margin Irregular margin
Floor Necrotic Slough in the
floor
Edges Everted Edges
Surrounding
Area
Shows nodules, ulcers
and irregularities
Size and
Extent
Large and Deep
BARIUM SWALLOW
ï‚¢ Outpouching of ulcer crater beyond the gastric
contour (exoluminal)
ï‚¢ Overhanging mucosa at the margins of a benign
gastric ulcer, project inwards towards the ulcer
ï‚¢ Regular/ Round Margin of the Ulcer Crater
ï‚¢ Converging mucosal folds towards the base of ulcer
ï‚¢ STOMACH SPOKE WHEEL PATTERN
ï‚¢ HAMPTON LINE: A thin millimetric radiolucent line
seen at the neck of a gastric ulcer in barium studies
ï‚¢ Deformed or absent duodenal cap
HAMPTON LINE: A thin millimetric radiolucent line seen at
the neck of a gastric ulcer in barium studies
STOMACH SPOKE` WHEEL
PATTERN
TESTS FOR H. PYLORI
ï‚¢ Noninvasive tests
ï‚— Serum or whole blood antibody tests
ï‚¢Immunoglobin G (IgG)
ï‚¢Urea breath test
ï‚¢ Patient drinks a carbon-enriched urea solution
ï‚¢ Excreted carbon dioxide is then measured
ï‚¢ Invasive tests
ï‚— Biopsy of stomach
ï‚— Rapid urease test
COMPLICATION
•Hemorrhage
•Perforation
•Penetration
•Narrowing and obstruction
HEMORRHAGE
ï‚— Blood vessels damaged as ulcer
erodes into the muscles of
stomach or duodenal wall
ï‚— Coffee ground vomitus or occult
blood in tarry stools
ï‚— Posterior wall duodenal ulcer
ï‚— Arteries involved
ï‚— GASTRIC ULCER erode LEFT
GASTRIC VESSELS and
SPLENIC VESSELS
ï‚— DUODENAL ULCER erodes
GASTRODUODENAL artery
PERFORATION
ï‚¢ Can erode through the entire wall
ï‚¢ Spillage of gastric/duodenal content and bacteria
into peritoneum leading to peritonitis
ï‚¢ Mostly associated with NSAIDs ulcers
ï‚¢ Anterior wall duodenal ulcer
PENETRATION
ï‚¢ Ulcers may erode through the entire thickness of
the gastric or duodenal wall into adjacent
abdominal organs
ï‚¢ Can involve the pancreas, bile ducts, liver, and the
small or large intestine.
ï‚¢ The pancreas is the most common site of
penetration
NARROWING AND OBSTRUCTION
ï‚¢ Hour glass contracture
ï‚— Cicatricial contracture of lesser curvature ulcer, dividing
the stomach in two compartments
ï‚¢ Teapot deformity
ï‚— Cicatrisation and shortening of lesser curve
ï‚¢ Pyloric stenosis
ï‚— Scarring and cicatrisation of first part of duodenum
ï‚¢ Persistent vomiting
MANAGEMENT
ï‚¢ Non-pharmacological
ï‚¢ Pharmacological
ï‚¢ Surgical
PHARMACOLOGICAL MANAGEMENT
ï‚¢ Provide pain relief
ï‚— Antacids and mucosa protectors
ï‚¢ Eradicate H. pylori infection
ï‚— Two antibiotics and one acid suppressor
ï‚¢ Heal ulcer
ï‚— Eradicate infection
ï‚— Protect until ulcer heals
ï‚¢ Prevent recurrence
ï‚— Decrease high acid stimulating foods in susceptible people
ï‚— Avoid use of potential ulcer causing drugs
ï‚— Stop smoking
AIM
NON-PHARMACOLOGICAL
• Avoid spicy food.
• Avoid Alcohol.
• Avoid Smoking.
• Avoid heavy meals.
• Encourage small frequent low caloric meals.
• Avoid ulcerating drugs e.g. NSAIDs, corticosteroids
HYPOSECRETORY DRUGS
ï‚¢ Proton Pump Inhibitors
ï‚— Suppress acid production
ï‚¢ H2-Receptor
Antagonists
ï‚— Block histamine-stimulated
gastric secretions
ï‚¢ Antacids
ï‚— Neutralizes acid and
prevents formation of
pepsin
ï‚— Give 2 hours after meals
and at bedtime
ï‚¢ Prostaglandin Analogs
ï‚— Reduce gastric acid and
enhances mucosal
resistance to injury
ï‚¢ Mucosal barrier
fortifiers
ï‚— Forms a protective coat
ï‚¢ Sucralfate
MEDICAL TREATMENT
ERADICATION THERAPY
ï‚¢ Directed against H. pylori
ï‚¢ Regimens
ï‚— Triple therapy for 2 weeks
ï‚¢ Omeprazole 20 mg twice daily or lansoprazole 30 mg twice daily
or pantoprazole 40 mg twice daily or esomeprazole 40 mg daily or
rabeprazole 20 mg daily
ï‚¢ Clarithromycin 500 mg twice daily
ï‚¢ Amoxicillin 1 g twice daily
ï‚— Quadruple therapy for 2 weeks
ï‚¢ Omeprazole 20 mg twice daily or pantoprazole 40 mg twice daily
or esomeprazole 40 mg daily or rabeprazole 20 mg daily
ï‚¢ Bismuth subsalicylate 525 mg twice daily
 Metronidazole 250–500 mg three times daily
ï‚¢ Tetracycline 500 mg four times daily
ï‚— The PPIs should be continued for 6 more weeks
SURGERY
ï‚¢ Indication
ï‚— Complicated ulcers
ï‚— Not responding to medical treatment
TYPES OF SURGICAL PROCEDURES
2.Gastroenterostomy
allows regurgitation of alkaline duodenal
contents into the stomach
• Gastrojejunostomy
1.Diversion of Acid Away from
the duodenum
•Billroth II
3.Reduce the secretory Potential of
Stomach
•Billroth I (gastric ulcer)
•Truncal vagotomy and drainage
•Highly selective vagotomy
•Truncal vagotomy and antrectomy
BILLROTH I GASTRECTOMY
Gastric ulcers
Distal portion of the
stomach is mobilised
and resected
The cut edge of the remnant is partially
closed from Lesser Curvature aspect
Stoma at greater curvature aspect
Gastroduodenal anastomosis done
BILLROTH II GASTRECTOMY
The lower portion of the
stomach is removed along
with the ulcer and the
remainder is anastomosed
to the jejunum
Recurrent ulceration is low
High Operative Mortality and
Morbidity
SEQUELAE OF PEPTIC ULCER SURGERY
ï‚¢ Recurrent Ulceration
ï‚¢ Small Stomach
Syndrome
ï‚¢ Bile Vomiting
ï‚¢ Early and Late
Dumping
ï‚¢ Post Vagotomy
Diarrhoea
ï‚¢ Malignant
Transformation
ï‚¢ Nutritional
Consequences
ï‚¢ Gall Stones
OTHER TYPES OF ULCER
ï‚¢ NSAIDs induced ulcers
ï‚— Antisecretory agents
ï‚¢ Stomal ulcers
ï‚— Prolonged course of antisecretory agents
ï‚¢ Zollinger- Ellison syndrome
ï‚— Proton pump inhibitors unless tumor can be managed
by surgery
MANAGEMENT OF COMPLICATIONS

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Peptic ulcer disease

  • 1. PEPTIC ULCER DISEASE Pukar K.C Kathmandu University School of Medical Sciences
  • 3. DEFINITIONS ï‚¢ Ulcer Breach in the mucosa of the GI tract that extends through the muscularis mucosa into submucosa or deeper ï‚¢ Erosion Epithelial disruption without breach of the muscularis mucosa ï‚¢ Peptic Ulcer disease Circumscribed ulcer that occurs in any part of the GI tract due to the aggressive action of acid and peptic juices.
  • 4. SITES OF ULCERS ï‚¢ First part of Duodenum ï‚¢ Lesser curve of stomach ï‚¢ Stoma following gastric surgery ï‚¢ Oesophagus ï‚¢ Gastric mucosa within Meckel’s Diverticulum
  • 5. ETIOLOGY ï‚¢ Helicobacter pylori infection ï‚¢ Chronic NSAIDs and Corticosteroids use ï‚¢ Cigarette smoking ï‚¢ Alcohol consumption ï‚¢ Zolinger-Ellison syndrome ï‚¢ Hyperparathyroidism and chronic renal failure
  • 7. ï‚¢ Zollinger- Ellison syndrome ï‚— Uncontrolled secretion of gastrin by tumor resulting massive acid production ï‚¢ NSAIDs use ï‚— Direct chemical irritation ï‚— Suppressing prostaglandin synthesis ï‚¢ Cigarette smoking ï‚— Impaired mucosal blood flow and healing ï‚¢ Hyperthyroidism and chronic renal failure ï‚— Hypercalcemia induced excessive gastrin secretion
  • 8. H. PYLORI ï‚¢ Flagella ï‚¢ Urease ï‚— Generates ammonia from endogenous urea and elevates pH ï‚¢ Adhesins ï‚— Enhance bacterial adherance to surface cells ï‚¢ Toxins ï‚— CagA gene
  • 11. Features Gastric ulcers Duodenal ulcers Incidence Less common More common Common Location Antrum, lesser cuvature Anterior wall*, 1st part Age group Middle age Middle or old age Male: Female ratio 1:1 4:1 Association with H. Pylori 65% 85%-100% Level of gastric acid secretion Mostly normal Mostly increased Malignancy Common Rare *Kissing ulcers: Both anterior and posterior wall ulcer of duodenum
  • 12. TYPES OF GASTRIC ULCER DAINTREE JOHNSON •Type I In the antrum, near lesser curvature Normal acid level •Type II Combined gastric and duodenal ulcer High acid level •Type III Prepyloric High acid level •Type IV Ulcer in the proximal stomach and Cardia Normal acid level 55% 25% 15% 5%
  • 13. FEW MORE ULCERS!!! ï‚¢ Stress ulcer ï‚— In association with shock, sepsis or severe trauma ï‚¢ Curling ulcer ï‚— In association with severe burns or trauma ï‚¢ Cushing’s ulcer ï‚— In patients with intracranial disease oor after neurosurgery
  • 14. CLINICAL PRESENTATION ï‚¢ Symptoms ï‚— Pain ï‚¢ Epigastric region, burning or aching type ï‚¢ May radiate to back ï‚— Heartburn, Nausea, vomiting, bloating, belching, water- brash ï‚— Alteration in weight ï‚— Haematemesis or Maelena  presents as anemia ï‚— Periodicity of symptoms ï‚¢ Significant past history ï‚¢ Clinical examination ï‚— Tender epigastrium ï‚— Features of complication, if present
  • 15. Gastric Ulcer Duodenal Ulcer Pain increased after food intake Pain relieved after food intake Periodicity less common Periodicity more common Haematemesis more common Melaena more common Weight loss common Weight gain occurs Equal in both sexes More in males
  • 16.
  • 17. INVESTIGATIONS ï‚¢ Esophagogastrodeodenoscopy (EGD) ï‚¢ Barium swallow ï‚¢ Urea Breath Testing
  • 18. ESOPHAGOGASTRODEODENOSCOPY It is fundamental that any gastric ulcer should be regarded as being Malignant, no matter how classically it resemble a benign gastric ulcer Multiple biopsies should be taken, as many as 10 well targeted biopsies
  • 19. ESOPHAGOGASTRODEODENOSCOPY ï‚— Endoscopic procedure ï‚— Visualizes ulcer crater ï‚— Ability to take tissue biopsy to R/O cancer and diagnose H. pylori
  • 20. BENIGN GASTRIC ULCER MUCOSAL FOLDS Converging folds Margin Regular Floor Granulation tissue in floor Edges NOT everted ,punched Surrounding Area Normal Size and Extent Small deep up to muscle layer
  • 21. MALIGNANT GASTRIC ULCER MUCOSAL FOLDS Effacing Mucosal folds Margin Irregular margin Floor Necrotic Slough in the floor Edges Everted Edges Surrounding Area Shows nodules, ulcers and irregularities Size and Extent Large and Deep
  • 22. BARIUM SWALLOW ï‚¢ Outpouching of ulcer crater beyond the gastric contour (exoluminal) ï‚¢ Overhanging mucosa at the margins of a benign gastric ulcer, project inwards towards the ulcer ï‚¢ Regular/ Round Margin of the Ulcer Crater ï‚¢ Converging mucosal folds towards the base of ulcer ï‚¢ STOMACH SPOKE WHEEL PATTERN ï‚¢ HAMPTON LINE: A thin millimetric radiolucent line seen at the neck of a gastric ulcer in barium studies ï‚¢ Deformed or absent duodenal cap
  • 23. HAMPTON LINE: A thin millimetric radiolucent line seen at the neck of a gastric ulcer in barium studies STOMACH SPOKE` WHEEL PATTERN
  • 24. TESTS FOR H. PYLORI ï‚¢ Noninvasive tests ï‚— Serum or whole blood antibody tests ï‚¢Immunoglobin G (IgG) ï‚¢Urea breath test ï‚¢ Patient drinks a carbon-enriched urea solution ï‚¢ Excreted carbon dioxide is then measured ï‚¢ Invasive tests ï‚— Biopsy of stomach ï‚— Rapid urease test
  • 25.
  • 27. HEMORRHAGE ï‚— Blood vessels damaged as ulcer erodes into the muscles of stomach or duodenal wall ï‚— Coffee ground vomitus or occult blood in tarry stools ï‚— Posterior wall duodenal ulcer ï‚— Arteries involved ï‚— GASTRIC ULCER erode LEFT GASTRIC VESSELS and SPLENIC VESSELS ï‚— DUODENAL ULCER erodes GASTRODUODENAL artery
  • 28. PERFORATION ï‚¢ Can erode through the entire wall ï‚¢ Spillage of gastric/duodenal content and bacteria into peritoneum leading to peritonitis ï‚¢ Mostly associated with NSAIDs ulcers ï‚¢ Anterior wall duodenal ulcer
  • 29. PENETRATION ï‚¢ Ulcers may erode through the entire thickness of the gastric or duodenal wall into adjacent abdominal organs ï‚¢ Can involve the pancreas, bile ducts, liver, and the small or large intestine. ï‚¢ The pancreas is the most common site of penetration
  • 30. NARROWING AND OBSTRUCTION ï‚¢ Hour glass contracture ï‚— Cicatricial contracture of lesser curvature ulcer, dividing the stomach in two compartments ï‚¢ Teapot deformity ï‚— Cicatrisation and shortening of lesser curve ï‚¢ Pyloric stenosis ï‚— Scarring and cicatrisation of first part of duodenum ï‚¢ Persistent vomiting
  • 32. PHARMACOLOGICAL MANAGEMENT ï‚¢ Provide pain relief ï‚— Antacids and mucosa protectors ï‚¢ Eradicate H. pylori infection ï‚— Two antibiotics and one acid suppressor ï‚¢ Heal ulcer ï‚— Eradicate infection ï‚— Protect until ulcer heals ï‚¢ Prevent recurrence ï‚— Decrease high acid stimulating foods in susceptible people ï‚— Avoid use of potential ulcer causing drugs ï‚— Stop smoking AIM
  • 33. NON-PHARMACOLOGICAL • Avoid spicy food. • Avoid Alcohol. • Avoid Smoking. • Avoid heavy meals. • Encourage small frequent low caloric meals. • Avoid ulcerating drugs e.g. NSAIDs, corticosteroids
  • 34. HYPOSECRETORY DRUGS ï‚¢ Proton Pump Inhibitors ï‚— Suppress acid production ï‚¢ H2-Receptor Antagonists ï‚— Block histamine-stimulated gastric secretions ï‚¢ Antacids ï‚— Neutralizes acid and prevents formation of pepsin ï‚— Give 2 hours after meals and at bedtime ï‚¢ Prostaglandin Analogs ï‚— Reduce gastric acid and enhances mucosal resistance to injury ï‚¢ Mucosal barrier fortifiers ï‚— Forms a protective coat ï‚¢ Sucralfate
  • 36.
  • 37. ERADICATION THERAPY ï‚¢ Directed against H. pylori ï‚¢ Regimens ï‚— Triple therapy for 2 weeks ï‚¢ Omeprazole 20 mg twice daily or lansoprazole 30 mg twice daily or pantoprazole 40 mg twice daily or esomeprazole 40 mg daily or rabeprazole 20 mg daily ï‚¢ Clarithromycin 500 mg twice daily ï‚¢ Amoxicillin 1 g twice daily ï‚— Quadruple therapy for 2 weeks ï‚¢ Omeprazole 20 mg twice daily or pantoprazole 40 mg twice daily or esomeprazole 40 mg daily or rabeprazole 20 mg daily ï‚¢ Bismuth subsalicylate 525 mg twice daily ï‚¢ Metronidazole 250–500 mg three times daily ï‚¢ Tetracycline 500 mg four times daily ï‚— The PPIs should be continued for 6 more weeks
  • 38. SURGERY ï‚¢ Indication ï‚— Complicated ulcers ï‚— Not responding to medical treatment
  • 39. TYPES OF SURGICAL PROCEDURES 2.Gastroenterostomy allows regurgitation of alkaline duodenal contents into the stomach • Gastrojejunostomy 1.Diversion of Acid Away from the duodenum •Billroth II 3.Reduce the secretory Potential of Stomach •Billroth I (gastric ulcer) •Truncal vagotomy and drainage •Highly selective vagotomy •Truncal vagotomy and antrectomy
  • 40. BILLROTH I GASTRECTOMY Gastric ulcers Distal portion of the stomach is mobilised and resected The cut edge of the remnant is partially closed from Lesser Curvature aspect Stoma at greater curvature aspect Gastroduodenal anastomosis done
  • 41. BILLROTH II GASTRECTOMY The lower portion of the stomach is removed along with the ulcer and the remainder is anastomosed to the jejunum Recurrent ulceration is low High Operative Mortality and Morbidity
  • 42. SEQUELAE OF PEPTIC ULCER SURGERY ï‚¢ Recurrent Ulceration ï‚¢ Small Stomach Syndrome ï‚¢ Bile Vomiting ï‚¢ Early and Late Dumping ï‚¢ Post Vagotomy Diarrhoea ï‚¢ Malignant Transformation ï‚¢ Nutritional Consequences ï‚¢ Gall Stones
  • 43. OTHER TYPES OF ULCER ï‚¢ NSAIDs induced ulcers ï‚— Antisecretory agents ï‚¢ Stomal ulcers ï‚— Prolonged course of antisecretory agents ï‚¢ Zollinger- Ellison syndrome ï‚— Proton pump inhibitors unless tumor can be managed by surgery