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PEPTIC ULCER DISEASES
Dr MAHES MANI ADHIKARI
General Surgery resident
Dhulikhel Hospital KUSMS
Surgical anatomy of Stomach
• Embryology
• Gross anatomy and gastric morphology
• Blood supply
• Lymphatic drainage
• Innervation
• Histology
Embryology
• Appear as fusiform dilatation of foregut
in the 4th week.
• Rotates 90* clockwise in longitudinal
axis
• Posterior wall elongates faster than
anterior wall- Greater and lesser
curvatures.
• Rotates in anteroposterior axis – caudal
or pyloric end towards right
Topography and relations
• Mobile
• Only fixed point of reference-
GEJ – left of midline behind 7th
costal cartilage @ T10 level
Divisions
Five arbitrarily defined regions are the:
• Cardia
• Fundus
• Body
• Antrum
• Pylorus
Blood supply
• Principle arterial supply – Coeliac trunk
• Left Gastric- ascending and descending
branch
• Hepatic- Right gastric , gastroduodenal
• Splenic- posterior gastric, short
gastrics, left gastroepiploic
• Venous drainage:
Lymphatics
• 4 zones:
• Zone I (inferior gastric) drains into the
subpyloric and omental nodes
• Zone II (splenic) drains into the
pancreaticosplenic nodes
• Zone III (superior gastric) drains into the
superior gastric nodes
• Zone IV (hepatic) drains into the suprapyloric
nodes
Innervation
• Extrinsic: Vagal innervations
• Intrinsic: the submucosal or
Meissner and the myenteric
or Auerbach plexus
Histology
• Mucosa- Epithelium
• Lamina propria
• Muscularis mucosa
• Submucosa
• Muscularis externa
• Serosa or visceral peritoneum
Physiology
• Regulation of gastric secretion
• Gastric peptides
• Gastric acid secretion
• Gastric motility
• Gastric barrier function
Regulation of gastric secretion
• Neural- Sympathetic or
parasympathetic
• Hormonal- Gastric peptides or
amines
• Vagal control of gastric acid secretion
and potentiation by histamine and
gastrin.
Gastrin
• Produced by G cells – gastric antrum
• G-34 (big gastrin), G-17 (little gastrin), and G-14 (minigastrin)
• Pentapeptide sequence at the carboxyl terminus - is the biologically active component
• Release - stimulated by food - protein
• Major hormonal regulator of the gastric phase of acid secretion after a meal
• Has considerable trophic effects on the parietal cells and gastric ECL cells
• Prolonged hypergastrinemia leads to
• mucosal hyperplasia
• an increase in the number of ECL cells
• under some circumstances, is associated with the development of gastric carcinoid
tumors
Phases of gastric acid secretion
Gastric Motility
• Regulated by extrinsic and intrinsic neural mechanisms and by myogenic control
• Fasting Gastric Motility
• Gastric pacemaker cells of cajal
• Slow waves travel at 3 cycles/minute in a circumferential and antegrade fashion
toward the pylorus
• Cyclical pattern of electrical activity - slow waves and electrical spikes, which has
been termed the Myoelectric Migrating Complex.
• Postprandial Gastric Motility
• Ingestion of a meal results in
• Decrease in the resting tone of the proximal stomach - receptive relaxation and
Fundus- gastric accommodation, respectively
• Repetitive forceful contractions of the midportion and antral portion of the stomach
• Food particles to be propelled against a closed pylorus, with subsequent retropulsion
of solids and liquids.
Gastric Barrier Function
• Gastric Mucus and Bicarbonate
• Gelatinous layer containing
• proteins, glycoproteins, mucopolysaccharide, and bicarbonate,
• Lines the superficial gastric epithelium
• Form a barrier between luminal contents and gastric mucosal cells.
• Neutralizes intraluminal acid - more physiologic pH at the mucosal surface
• maintains a steep pH gradient across it, which ranges from a pH of 2 on the luminal
side to a pH of 7 on the epithelial side
• Inhibitors of cyclooxygenase (COX), such as aspirin or nonsteroidal anti-inflammatory
drugs (NSAIDs) – inhibit mucus production
• Blood flow
• Reduced by more than 75%, marked mucosal injury results
• Injury exacerbated in the presence of luminal acid
• Restitution or reconstitution
• injured surface epithelial cells are replaced rapidly by the migration of surface
mucous cells located along the basement membranes.
• It occurs within minutes and does not require cell division
Peptic ulcer disease
• Epidemiology
• Pathogenesis
• Duodenal ulcers
• Gastric ulcers
• Both types tend to occur near mucosal junctions.
• Duodenal ulcers – duodenal-pyloric junction
• Gastric ulcers – oxynticantral junction, the antral-pyloric junction, or the
esophagogastric junction
Epidemiology
• defined as erosions in the gastric or duodenal mucosa that extend
through the muscularis mucosae
• Surgical treatment has declined since the advent of different acid
suppression strategies and eradication of H. pylori
• Complications – Bleeding, perforation and obstruction
• Perforation carries the highest mortality risk - upto 30%
Pathogenesis
• Peptic ulcers are caused by increased aggressive factors, decreased defensive factors, or
both.
• Damaging factors
• Hydrochloric acid secretion,
• Pepsins,
• Ethanol ingestion,
• Smoking,
• Duodenal reflux of bile,
• Ischemia,
• NSAIDs,
• Hypoxia,
• Most notably, H. pylori infection
Helicobacter pylori
• 80% to 95% of duodenal ulcers and
• Approximately 75% of gastric ulcers
• Primary causative factor in the pathogenesis of PUD
• Spiral or helical gram-negative rod with 4-6 flagella
that resides
• Resides in gastric-type epithelium within or beneath
the mucous layer
• Infection was associated with a twofold
• Increased risk of developing gastric cancer
Immunohistochemical staining
of H. pylori (brown) from a gastric biopsy
• Potent producer of urease
• Creates an alkaline microenvironment
• Splits urea into ammonia and bicarbonate, which is capable of splitting, in the setting
of an acidic gastric milieu microaerophilic
• Can live only in gastric epithelium
• Can also be found in heterotopic gastric mucosa
• In the proximal esophagus, in barrett esophagus,
• In gastric metaplasia in the duodenum,
• Within a meckel’s diverticulum, and
• In heterotopic gastric mucosa in the rectum
• Mechanisms responsible for H. pylori–induced GI injury
1. Production of toxic products that cause local tissue injury
• Ammonia, cytotoxins, mucinase, phospholipases
2. Induction of a local mucosal immune response
3. Increased gastrin levels with a resultant increase in acid secretion
• Basal and stimulated gastrin level increased – reduced antral D cells
4. Gastric metaplasia occurring in the duodenum
NSAIDs
• Risk for bleeding and ulceration is proportional to the daily dosage of NSAIDs
• Absorbed through the stomach and small intestine
• As systemic inhibitors of the cyclooxygenase enzymes
• Rate-limiting step of prostaglandin synthesis in the GI tract.
• Prostaglandins promote gastric and duodenal mucosal protection via numerous
mechanisms,
• Including increasing mucin and bicarbonate secretion
• And increasing blood flow to the mucosal endothelium
• a 2-fold to 10-fold increased risk for GI complications
• The risk for mucosal injury or ulceration is roughly proportional to the anti-inflammatory
effect associated with each NSAID
• H. pylori ulcers, - duodenum,
• NSAID-induced ulcers - stomach.
• H. pylori ulcers - chronic active gastritis,
• Whereas gastritis is not frequently found with NSAID-induced ulcers, occurring only
approximately 25% of the time.
• When NSAID use is discontinued, the ulcers usually do not recur.
• Acid
• Important but likely noncausative role
• In duodenal ulcers, there is a large overlap of acid levels between patients with ulcers
and normal subjects.
• Almost 70% of patients with duodenal ulcers have an acid output within the normal
range.
• For types I and IV gastric ulcers, which are not associated with excessive acid secretion,
acid acts as an important cofactor, exacerbating the underlying ulcer damage and
attenuating the ability of the stomach to heal.
• For patients with type II or III gastric ulcers, gastric acid hypersecretion seems to be more
common, and consequently these ulcers behave more like duodenal ulcers
Duodenal ulcers
• Requirements are acid and pepsin secretion in combination with infection by H. pylori or
ingestion of NSAIDs more common
• Secretory abnormalities relate to
• Decreased bicarbonate secretion,
• Increased nocturnal acid secretion,
• Increased duodenal acid load, and
• Increased daytime acid secretion
Gastric ulcers
• Occur anywhere in the stomach,
usually present on the lesser curvature
• Peak incidence of gastric ulcers
occurrence is between 55 and 65 years
of age
• Presence of acid appears to be
essential
• Rapid healing follows
• Antacid therapy,
• Antisecretory therapy, or
• Vagotomy,
• Even when the lesion-bearing portion of
the stomach is left intact
Clinical Manifestations
• Duodenal Ulcers
• Abdominal Pain
• most common symptom
• well-localized mid-epigastric
• Frequently relieved by food
• presence of constant pain suggests
• deeper penetration of the ulcer
• and referral of pain to the back – penetration into the pancreas
• Diffuse peritoneal irritation - free perforation.
• Perforation
• About 5%
• Penetrate through the duodenum into the free peritoneal cavity
• Elicit a chemical peritonitis
• Patient can typically recall the exact time of onset of abdominal pain
• Frequently accompanied by fever, tachycardia, dehydration, and ileus.
• Abdominal examination- exquisite tenderness, rigidity, and rebound
• Demonstration of free air underneath the diaphragm on an upright chest
radiograph.
• Bleeding
• Most common cause of death in patients
• Gastroduodenal artery
• Bleeding duodenal ulcers account for about 25% of all upper GI bleeding
patients.
• Obstruction.
• Acute inflammation of the duodenum - functional gastric outlet obstruction
• Manifested by
• Delayed gastric emptying, anorexia, or nausea accompanied by vomiting.
• Chronic inflammation of the duodenum - recurrent episodes of healing followed
by repair and scarring with, ultimately, fibrosis and stenosis of the duodenal
lumen
• Painless vomiting of large volumes of gastric contents with similar metabolic
abnormalities as seen in the acute situation.
• The stomach can become massively dilated in this setting and it rapidly loses its
muscular tone.
• Marked weight loss and malnutrition are also common in this situation.
• Gastric ulcer
• Clinical challenge in that it is often impossible to differentiate between gastric
carcinoma and benign ulcers
• Recurrent episodes
• Surgical intervention is required in 8% to 20%
• Most frequent - perforation
• along the anterior aspect of the lesser curvature.
• larger ulcers are associated with more morbidity and higher mortality rates
• Hemorrhage - 35% to 40% - at some point during the course of gastric ulceration
• Hemorrhage and Gastric Outlet Obstruction- type 2 and type 3 gastric ulcers
• Thank you!

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Peptic ulcer disease

  • 1. PEPTIC ULCER DISEASES Dr MAHES MANI ADHIKARI General Surgery resident Dhulikhel Hospital KUSMS
  • 2. Surgical anatomy of Stomach • Embryology • Gross anatomy and gastric morphology • Blood supply • Lymphatic drainage • Innervation • Histology
  • 3. Embryology • Appear as fusiform dilatation of foregut in the 4th week. • Rotates 90* clockwise in longitudinal axis • Posterior wall elongates faster than anterior wall- Greater and lesser curvatures. • Rotates in anteroposterior axis – caudal or pyloric end towards right
  • 4. Topography and relations • Mobile • Only fixed point of reference- GEJ – left of midline behind 7th costal cartilage @ T10 level
  • 5. Divisions Five arbitrarily defined regions are the: • Cardia • Fundus • Body • Antrum • Pylorus
  • 6. Blood supply • Principle arterial supply – Coeliac trunk • Left Gastric- ascending and descending branch • Hepatic- Right gastric , gastroduodenal • Splenic- posterior gastric, short gastrics, left gastroepiploic
  • 8. Lymphatics • 4 zones: • Zone I (inferior gastric) drains into the subpyloric and omental nodes • Zone II (splenic) drains into the pancreaticosplenic nodes • Zone III (superior gastric) drains into the superior gastric nodes • Zone IV (hepatic) drains into the suprapyloric nodes
  • 9. Innervation • Extrinsic: Vagal innervations • Intrinsic: the submucosal or Meissner and the myenteric or Auerbach plexus
  • 10. Histology • Mucosa- Epithelium • Lamina propria • Muscularis mucosa • Submucosa • Muscularis externa • Serosa or visceral peritoneum
  • 11. Physiology • Regulation of gastric secretion • Gastric peptides • Gastric acid secretion • Gastric motility • Gastric barrier function
  • 12. Regulation of gastric secretion • Neural- Sympathetic or parasympathetic • Hormonal- Gastric peptides or amines
  • 13.
  • 14. • Vagal control of gastric acid secretion and potentiation by histamine and gastrin.
  • 15. Gastrin • Produced by G cells – gastric antrum • G-34 (big gastrin), G-17 (little gastrin), and G-14 (minigastrin) • Pentapeptide sequence at the carboxyl terminus - is the biologically active component • Release - stimulated by food - protein • Major hormonal regulator of the gastric phase of acid secretion after a meal
  • 16. • Has considerable trophic effects on the parietal cells and gastric ECL cells • Prolonged hypergastrinemia leads to • mucosal hyperplasia • an increase in the number of ECL cells • under some circumstances, is associated with the development of gastric carcinoid tumors
  • 17.
  • 18. Phases of gastric acid secretion
  • 19. Gastric Motility • Regulated by extrinsic and intrinsic neural mechanisms and by myogenic control • Fasting Gastric Motility • Gastric pacemaker cells of cajal • Slow waves travel at 3 cycles/minute in a circumferential and antegrade fashion toward the pylorus • Cyclical pattern of electrical activity - slow waves and electrical spikes, which has been termed the Myoelectric Migrating Complex.
  • 20. • Postprandial Gastric Motility • Ingestion of a meal results in • Decrease in the resting tone of the proximal stomach - receptive relaxation and Fundus- gastric accommodation, respectively • Repetitive forceful contractions of the midportion and antral portion of the stomach • Food particles to be propelled against a closed pylorus, with subsequent retropulsion of solids and liquids.
  • 21. Gastric Barrier Function • Gastric Mucus and Bicarbonate • Gelatinous layer containing • proteins, glycoproteins, mucopolysaccharide, and bicarbonate, • Lines the superficial gastric epithelium • Form a barrier between luminal contents and gastric mucosal cells. • Neutralizes intraluminal acid - more physiologic pH at the mucosal surface • maintains a steep pH gradient across it, which ranges from a pH of 2 on the luminal side to a pH of 7 on the epithelial side • Inhibitors of cyclooxygenase (COX), such as aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) – inhibit mucus production
  • 22. • Blood flow • Reduced by more than 75%, marked mucosal injury results • Injury exacerbated in the presence of luminal acid • Restitution or reconstitution • injured surface epithelial cells are replaced rapidly by the migration of surface mucous cells located along the basement membranes. • It occurs within minutes and does not require cell division
  • 23. Peptic ulcer disease • Epidemiology • Pathogenesis • Duodenal ulcers • Gastric ulcers • Both types tend to occur near mucosal junctions. • Duodenal ulcers – duodenal-pyloric junction • Gastric ulcers – oxynticantral junction, the antral-pyloric junction, or the esophagogastric junction
  • 24. Epidemiology • defined as erosions in the gastric or duodenal mucosa that extend through the muscularis mucosae • Surgical treatment has declined since the advent of different acid suppression strategies and eradication of H. pylori • Complications – Bleeding, perforation and obstruction • Perforation carries the highest mortality risk - upto 30%
  • 25. Pathogenesis • Peptic ulcers are caused by increased aggressive factors, decreased defensive factors, or both. • Damaging factors • Hydrochloric acid secretion, • Pepsins, • Ethanol ingestion, • Smoking, • Duodenal reflux of bile, • Ischemia, • NSAIDs, • Hypoxia, • Most notably, H. pylori infection
  • 26. Helicobacter pylori • 80% to 95% of duodenal ulcers and • Approximately 75% of gastric ulcers • Primary causative factor in the pathogenesis of PUD • Spiral or helical gram-negative rod with 4-6 flagella that resides • Resides in gastric-type epithelium within or beneath the mucous layer • Infection was associated with a twofold • Increased risk of developing gastric cancer Immunohistochemical staining of H. pylori (brown) from a gastric biopsy
  • 27. • Potent producer of urease • Creates an alkaline microenvironment • Splits urea into ammonia and bicarbonate, which is capable of splitting, in the setting of an acidic gastric milieu microaerophilic • Can live only in gastric epithelium • Can also be found in heterotopic gastric mucosa • In the proximal esophagus, in barrett esophagus, • In gastric metaplasia in the duodenum, • Within a meckel’s diverticulum, and • In heterotopic gastric mucosa in the rectum
  • 28. • Mechanisms responsible for H. pylori–induced GI injury 1. Production of toxic products that cause local tissue injury • Ammonia, cytotoxins, mucinase, phospholipases 2. Induction of a local mucosal immune response 3. Increased gastrin levels with a resultant increase in acid secretion • Basal and stimulated gastrin level increased – reduced antral D cells 4. Gastric metaplasia occurring in the duodenum
  • 29. NSAIDs • Risk for bleeding and ulceration is proportional to the daily dosage of NSAIDs • Absorbed through the stomach and small intestine • As systemic inhibitors of the cyclooxygenase enzymes • Rate-limiting step of prostaglandin synthesis in the GI tract. • Prostaglandins promote gastric and duodenal mucosal protection via numerous mechanisms, • Including increasing mucin and bicarbonate secretion • And increasing blood flow to the mucosal endothelium
  • 30. • a 2-fold to 10-fold increased risk for GI complications • The risk for mucosal injury or ulceration is roughly proportional to the anti-inflammatory effect associated with each NSAID • H. pylori ulcers, - duodenum, • NSAID-induced ulcers - stomach. • H. pylori ulcers - chronic active gastritis, • Whereas gastritis is not frequently found with NSAID-induced ulcers, occurring only approximately 25% of the time. • When NSAID use is discontinued, the ulcers usually do not recur.
  • 31. • Acid • Important but likely noncausative role • In duodenal ulcers, there is a large overlap of acid levels between patients with ulcers and normal subjects. • Almost 70% of patients with duodenal ulcers have an acid output within the normal range. • For types I and IV gastric ulcers, which are not associated with excessive acid secretion, acid acts as an important cofactor, exacerbating the underlying ulcer damage and attenuating the ability of the stomach to heal. • For patients with type II or III gastric ulcers, gastric acid hypersecretion seems to be more common, and consequently these ulcers behave more like duodenal ulcers
  • 32. Duodenal ulcers • Requirements are acid and pepsin secretion in combination with infection by H. pylori or ingestion of NSAIDs more common • Secretory abnormalities relate to • Decreased bicarbonate secretion, • Increased nocturnal acid secretion, • Increased duodenal acid load, and • Increased daytime acid secretion
  • 33. Gastric ulcers • Occur anywhere in the stomach, usually present on the lesser curvature • Peak incidence of gastric ulcers occurrence is between 55 and 65 years of age • Presence of acid appears to be essential • Rapid healing follows • Antacid therapy, • Antisecretory therapy, or • Vagotomy, • Even when the lesion-bearing portion of the stomach is left intact
  • 34. Clinical Manifestations • Duodenal Ulcers • Abdominal Pain • most common symptom • well-localized mid-epigastric • Frequently relieved by food • presence of constant pain suggests • deeper penetration of the ulcer • and referral of pain to the back – penetration into the pancreas • Diffuse peritoneal irritation - free perforation.
  • 35. • Perforation • About 5% • Penetrate through the duodenum into the free peritoneal cavity • Elicit a chemical peritonitis • Patient can typically recall the exact time of onset of abdominal pain • Frequently accompanied by fever, tachycardia, dehydration, and ileus. • Abdominal examination- exquisite tenderness, rigidity, and rebound • Demonstration of free air underneath the diaphragm on an upright chest radiograph.
  • 36. • Bleeding • Most common cause of death in patients • Gastroduodenal artery • Bleeding duodenal ulcers account for about 25% of all upper GI bleeding patients.
  • 37. • Obstruction. • Acute inflammation of the duodenum - functional gastric outlet obstruction • Manifested by • Delayed gastric emptying, anorexia, or nausea accompanied by vomiting. • Chronic inflammation of the duodenum - recurrent episodes of healing followed by repair and scarring with, ultimately, fibrosis and stenosis of the duodenal lumen • Painless vomiting of large volumes of gastric contents with similar metabolic abnormalities as seen in the acute situation. • The stomach can become massively dilated in this setting and it rapidly loses its muscular tone. • Marked weight loss and malnutrition are also common in this situation.
  • 38. • Gastric ulcer • Clinical challenge in that it is often impossible to differentiate between gastric carcinoma and benign ulcers • Recurrent episodes • Surgical intervention is required in 8% to 20% • Most frequent - perforation • along the anterior aspect of the lesser curvature. • larger ulcers are associated with more morbidity and higher mortality rates • Hemorrhage - 35% to 40% - at some point during the course of gastric ulceration • Hemorrhage and Gastric Outlet Obstruction- type 2 and type 3 gastric ulcers