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Presenter: AnilKr. Yadav
PATHOLOGY
OF
PEPTIC ULCER
ResourceFaculty: Dr. ParichaUpadhyaya
Presenter:Anil Kr. Yadav
OBJECTIVES
o Definition and pathogenesis
of Peptic Ulcer
o Morphology of Peptic Ulcer
o Complications
DEFINITION
Ulcer is defined as disruption of the mucosal integrity of
stomach and/or duodenum leading to a local defect or
excavation due to active inflammation.
Erosion differs from an ulcer in being partial thickness
mucosal defect.
Peptic ulcers are chronic most often solitary lesions that
occur in any portion of GIT exposed to the aggressive action
of acid-peptic juices.
PROGRESSION
PATHOGENESIS
Aggressive factors Defensive factors
Gastric acidity
Peptic enzymes
Surface mucus secretion
Bicarbonate secretion into mucus
Mucosal blood flow
Apical surface membrane transport
Epithelial regenerative capacity
Elaboration of PG
INJURY
PEPTIC ULCER
H. Pylori infection
NSAID
Tobacco
Alcohol
Gastric hyperacidity
Duodenal-gastric reflux
Impaired defenses
Ischemia
Shock
Delayed gastric emptying
Pathology of Peptic Ulcer Disease
RISK FACTORS FOR PUD
H. Pylori infection
NSAIDs
Cigarette use
COPD
Ilicit drugs like cocaine
Alcoholic cirrhosis
Psychological stress
Endocrine cell hyperplasia
ZE syndrome
Viral infection (CMV, HSV)
Organism attached to mucus-secreting cells of
gastric mucosa by adhesins like BabA and SabA
H. Pylori transmitted by fecal-oral/ oral-oral route
In the stomach it swims in viscous mucus due to flagella
Ammonia neutralizes HCl in stomach
Production of large amount of ammonia from urea
by bacterial urease
Organism survival
Inflammatory response
Damage to mucus
Gastritis and peptic ulcers
Pathology of Peptic Ulcer Disease
Pathology of Peptic Ulcer Disease
NSAIDS
Membrane phospholipids
Phospholipase A2
Arachidonic acid
COX
PG depletion
Epithelial effects
Increase in HCl secretion
Decrease mucin secretion
Decrease HCO3- secretion
Decrease surface active
phospholipids secretion
Decrease epithelial cell
proliferation
NSAIDs
inhibits
Endothelial effects
Stasis ischemia
SITES OF PEPTIC ULCERS
Duodenum: 1st portion, Anterior wall
Stomach: usually antrum, lesser curvature
(common), anterior and posterior wall, greater
curvature (less common)
In the margins of a gastroenterostomy
(stomal ulcer)
In the duodenum, stomach or jejunum of
patients with Zollinger-Ellison syndrome
With or adjacent to a Meckels diverticulum.
MORPHOLOGY
GROSS
Round to oval, sharply punched-out defect
Mucosal margin usually level with the
surrounding mucosa or only slightly elevated
Radiating mucosal folds
Base is smooth and clear, owing to the peptic
digestion of exudates
Pathology of Peptic Ulcer Disease
MORPHOLOGY
MICROSCOPY
Four zones are seen
Layer of necrotic fibrinoid debris
Zone of acute inflammatory infiltrate
(neutrophils)
Active granulation tissue with
mononuclear leukocytes
Fibrous scarring
CLINICAL FEATURES
Epigastric pain
Dyspepsia, including belching, bloating, distention,
and fatty food intolerance
Heartburn
Chest discomfort
Hematemesis or melena resulting from
gastrointestinal bleeding
COMPLICATIONS
 Hemorrhage
Blood vessels damaged as ulcer erodes into the muscles GIT
Coffee ground vomitus or occult blood in tarry stools
 Perforation
An ulcer can erode through the entire wall
Bacteria and partially digested food spill into peritoneum
:Peritonitis
 Narrowing and obstruction (pyloric)
Swelling and scarring can cause obstruction of food leaving
stomach : Repeated vomiting
Pathology of Peptic Ulcer Disease
Pathology of Peptic Ulcer Disease
REFERENCES
Pathology of Peptic Ulcer Disease

More Related Content

Pathology of Peptic Ulcer Disease

  • 1. Presenter: AnilKr. Yadav PATHOLOGY OF PEPTIC ULCER ResourceFaculty: Dr. ParichaUpadhyaya Presenter:Anil Kr. Yadav
  • 2. OBJECTIVES o Definition and pathogenesis of Peptic Ulcer o Morphology of Peptic Ulcer o Complications
  • 3. DEFINITION Ulcer is defined as disruption of the mucosal integrity of stomach and/or duodenum leading to a local defect or excavation due to active inflammation. Erosion differs from an ulcer in being partial thickness mucosal defect. Peptic ulcers are chronic most often solitary lesions that occur in any portion of GIT exposed to the aggressive action of acid-peptic juices.
  • 5. PATHOGENESIS Aggressive factors Defensive factors Gastric acidity Peptic enzymes Surface mucus secretion Bicarbonate secretion into mucus Mucosal blood flow Apical surface membrane transport Epithelial regenerative capacity Elaboration of PG
  • 6. INJURY PEPTIC ULCER H. Pylori infection NSAID Tobacco Alcohol Gastric hyperacidity Duodenal-gastric reflux Impaired defenses Ischemia Shock Delayed gastric emptying
  • 8. RISK FACTORS FOR PUD H. Pylori infection NSAIDs Cigarette use COPD Ilicit drugs like cocaine Alcoholic cirrhosis Psychological stress Endocrine cell hyperplasia ZE syndrome Viral infection (CMV, HSV)
  • 9. Organism attached to mucus-secreting cells of gastric mucosa by adhesins like BabA and SabA H. Pylori transmitted by fecal-oral/ oral-oral route In the stomach it swims in viscous mucus due to flagella Ammonia neutralizes HCl in stomach Production of large amount of ammonia from urea by bacterial urease Organism survival Inflammatory response Damage to mucus Gastritis and peptic ulcers
  • 12. NSAIDS Membrane phospholipids Phospholipase A2 Arachidonic acid COX PG depletion Epithelial effects Increase in HCl secretion Decrease mucin secretion Decrease HCO3- secretion Decrease surface active phospholipids secretion Decrease epithelial cell proliferation NSAIDs inhibits Endothelial effects Stasis ischemia
  • 13. SITES OF PEPTIC ULCERS Duodenum: 1st portion, Anterior wall Stomach: usually antrum, lesser curvature (common), anterior and posterior wall, greater curvature (less common) In the margins of a gastroenterostomy (stomal ulcer) In the duodenum, stomach or jejunum of patients with Zollinger-Ellison syndrome With or adjacent to a Meckels diverticulum.
  • 14. MORPHOLOGY GROSS Round to oval, sharply punched-out defect Mucosal margin usually level with the surrounding mucosa or only slightly elevated Radiating mucosal folds Base is smooth and clear, owing to the peptic digestion of exudates
  • 16. MORPHOLOGY MICROSCOPY Four zones are seen Layer of necrotic fibrinoid debris Zone of acute inflammatory infiltrate (neutrophils) Active granulation tissue with mononuclear leukocytes Fibrous scarring
  • 17. CLINICAL FEATURES Epigastric pain Dyspepsia, including belching, bloating, distention, and fatty food intolerance Heartburn Chest discomfort Hematemesis or melena resulting from gastrointestinal bleeding
  • 18. COMPLICATIONS Hemorrhage Blood vessels damaged as ulcer erodes into the muscles GIT Coffee ground vomitus or occult blood in tarry stools Perforation An ulcer can erode through the entire wall Bacteria and partially digested food spill into peritoneum :Peritonitis Narrowing and obstruction (pyloric) Swelling and scarring can cause obstruction of food leaving stomach : Repeated vomiting

Editor's Notes