ACID PEPTIC DISEASE
INTRODUCTION:
✓ Ulcer in the lower oesophagus, stomach, or duodenum, in the jejunum after surgical
anastomosis to stomach, and in the ileum adjacent to the Meckel’s diverticulum.
✓ 90% of the peptic ulcers are due to Helicobacter pylori infection or NSAIDs use.
ETIOLOGY:
✓ HEREDITARY
• Strong family history – gastric ulcers
✓ ACID PEPSIN v/s MUCOSAL RESISTANCE
• Acid & pepsin of gastric juice – digestion of the mucosa
• Gastric hypersecretion:
Zollinger-Ellison syndrome – very high acid secretion.
• Mucosal resistance – gastric mucosal barrier:
Tight intercellular junctions, surface lipoprotein layer –
mechanical barrier.
Mucus – impedes the diffusion of ions & molecules – pepsin.
Submucosal area- removing toxic metabolic by-products.
✓ PROSTAGLANDINS – central role
Release of mucosal bicarbonates and mucous.
Inhibit parietal cell secretion.
Maintaining mucosal blood flow.
✓ FACTORS REDUCING MUCOSAL RESISTANCE
Aspirin – damages the membrane & tight junctions, inhibits prostaglandin
synthesis.
Drugs – rheumatoid arthritis.
Helicobacter pylori.
Reflux of bile & intestinal contents into stomach – poorly functioning
pyloric sphincter.
✓ Helicobacter pylori:
Gram-negative bacillus – produces mucosal damage.
Gastritis, gastric adenocarcinoma, gastritis & dyspepsia.
Poor socio-economic conditions & family overcrowding.
Oral-oral & faeco-oral route.
, PATHOGENESIS:
Combination of ammonia and water
Formation of free hydroxyl radicals
Free radicals disrupt epithelial integrity
Produces an ulcer
Ulcer attracts neutrophils & monocytes towards itself
Monocytes liberate IL-1 & TNF which in turn disrupts
the epithelial integrity
It liberates proteinases & phospholipases
Disrupts the protective mucosal coat covering the gastric epithelium
Thereby allowing the acid to disrupt the gastric epithelium.
CLINICAL FEATURES:
Chronic condition – spontaneous relapses & remissions lasting for decades.
Recurrent abdominal pain with three notable characters – most common:
▪ Localisation to the epigastrium: Referred to epigastrium so sharply –
pointing sign, burning nature.
▪ Relationship to food: Occurs on empty stomach (hunger pain) & is relieved
by food or antacids.
INTRODUCTION:
✓ Ulcer in the lower oesophagus, stomach, or duodenum, in the jejunum after surgical
anastomosis to stomach, and in the ileum adjacent to the Meckel’s diverticulum.
✓ 90% of the peptic ulcers are due to Helicobacter pylori infection or NSAIDs use.
ETIOLOGY:
✓ HEREDITARY
• Strong family history – gastric ulcers
✓ ACID PEPSIN v/s MUCOSAL RESISTANCE
• Acid & pepsin of gastric juice – digestion of the mucosa
• Gastric hypersecretion:
Zollinger-Ellison syndrome – very high acid secretion.
• Mucosal resistance – gastric mucosal barrier:
Tight intercellular junctions, surface lipoprotein layer –
mechanical barrier.
Mucus – impedes the diffusion of ions & molecules – pepsin.
Submucosal area- removing toxic metabolic by-products.
✓ PROSTAGLANDINS – central role
Release of mucosal bicarbonates and mucous.
Inhibit parietal cell secretion.
Maintaining mucosal blood flow.
✓ FACTORS REDUCING MUCOSAL RESISTANCE
Aspirin – damages the membrane & tight junctions, inhibits prostaglandin
synthesis.
Drugs – rheumatoid arthritis.
Helicobacter pylori.
Reflux of bile & intestinal contents into stomach – poorly functioning
pyloric sphincter.
✓ Helicobacter pylori:
Gram-negative bacillus – produces mucosal damage.
Gastritis, gastric adenocarcinoma, gastritis & dyspepsia.
Poor socio-economic conditions & family overcrowding.
Oral-oral & faeco-oral route.
, PATHOGENESIS:
Combination of ammonia and water
Formation of free hydroxyl radicals
Free radicals disrupt epithelial integrity
Produces an ulcer
Ulcer attracts neutrophils & monocytes towards itself
Monocytes liberate IL-1 & TNF which in turn disrupts
the epithelial integrity
It liberates proteinases & phospholipases
Disrupts the protective mucosal coat covering the gastric epithelium
Thereby allowing the acid to disrupt the gastric epithelium.
CLINICAL FEATURES:
Chronic condition – spontaneous relapses & remissions lasting for decades.
Recurrent abdominal pain with three notable characters – most common:
▪ Localisation to the epigastrium: Referred to epigastrium so sharply –
pointing sign, burning nature.
▪ Relationship to food: Occurs on empty stomach (hunger pain) & is relieved
by food or antacids.
