Peptic Ulcer Disease and Premalignant Conditions

Peptic Ulcer Disease and Helicobacter pylori

General Information
  • Peptic ulcer disease is often caused by Helicobacter pylori (H. pylori).
  • H. pylori is an extracellular bacterium, unlike Tropherma whipplei in Whipple's disease, which is intracellular.
  • H. pylori causes type B gastritis, the leading cause of peptic ulcer disease.
Microbiology of H. pylori
  • Gram-negative coccobacillus: It can switch between coccoid and bacillus forms.
  • Non-sporing: Eradication with antibiotics is possible since it won't come back as spores.
  • Spread: Via the fecal-oral route, explaining the higher incidence in developing countries.
  • Microaerophilic: Requires less oxygen and can survive in the stomach environment.
Mechanism of Action
  • Urease Production: H. pylori produces urease, which generates ammonia.
  • Ammonia's Effect: Ammonia is alkaline and irritates G cells.
  • G Cell Stimulation: Leads to excessive gastrin production.
  • Hyperchlorhydria: Excessive gastrin stimulates parietal cells, leading to increased acid production (hyperchlorhydria).
  • Impact on Duodenum: Excess acid flows into the duodenum, causing duodenal ulcers because the duodenum lacks the stomach's protective prostaglandins.
Duodenal Ulcer Symptoms
  • Epigastric Pain: Occurs when the stomach empties, typically two hours after eating.
  • Snacking: Patients often snack to alleviate pain, leading to weight gain due to increased calorie and fat intake.
  • Hypergastrinemia and Hyperchlorhydria: Both conditions are present.
Achlorhydria and Ulcers
  • Even with less acid (achlorhydria), ulcers can occur due to weakened stomach defense mechanisms.
Diagnosis of H. pylori
  • Initial Test: Breath urea test is preferred as a non-invasive screening test.
  • Eradication Test: Breath urea test is also used to determine the eradication of H. pylori infection.
  • Urease Test (CLO test): An invasive test involving a stomach scraping during endoscopy.
    • Biopsy: Warthensari stain (silver stain) is of historical importance and is not typically used for diagnosis nowdays.
Treatment
  • Antibiotics:
    • Clarithromycin and amoxicillin combination is commonly prescribed for two weeks.
    • Ampicillin can be used but has a higher incidence of diarrhea.
    • Tetracycline and metronidazole (or ornidazole) can also be used in combination.
    • Erythromycin has not been shown to be effective against H. pylori.
  • PPI: Proton pump inhibitors are given for 4-6 weeks to heal ulcers.
  • Triple Therapy: Two antibiotics with a PPI.
  • Quadruple Therapy: Two antibiotics, PPI, and a surface protective agent like bismuth.
    • Bismuth reduces acid mucosa contact time.

Type A Gastritis

Characteristics
  • Hypergastrinemia: Similar to type B gastritis but with achlorhydria (less acid production).
  • Etiology: Autoimmune, with antibodies against parietal cells.
  • B12 Deficiency: Parietal cells produce intrinsic factor, so their destruction leads to B12 deficiency, causing pernicious anemia or megaloblastic anemia.
  • Pre-Malignant Condition: Gastric ulcers develop due to weakened stomach defense mechanisms.

Gastric vs. Duodenal Ulcers

Associations
  • Gastric Ulcer: Related to blood group A.
  • Duodenal Ulcer: Related to blood group O (remember "DUO").
Location
  • Gastric Ulcer: Commonly on the lesser curvature near incisura angularis (Type 1 gastric ulcer based on Johnson classification).
  • Duodenal Ulcer: Commonly in the first part of the duodenum, known as the duodenal cap.
Presentation
  • Gastric Ulcer:
    • Pain starts soon after eating.
    • Patients avoid food, leading to weight loss.
    • Often consume milk, curd, or soup.
  • Duodenal Ulcer:
    • Pain occurs every two hours (stomach emptying time).
    • Patients snack frequently, leading to weight gain.
Investigation
  • Upper GI Endoscopy: Used to visualize the ulcer and perform a biopsy (especially for gastric ulcers to rule out malignancy).
  • Urease Test: Often performed in Indian settings due to the higher incidence of H. pylori.
Treatment
  • PPIs: Given for 4-6 weeks for ulcer healing.
  • Antibiotics: Prescribed based on urease test results.
Refractory Peptic Ulcer Disease
  • Consider Zollinger-Ellison Syndrome: Suspect this if the ulcer heals with PPIs but recurs upon stopping them.
  • Secretory Diarrhea: A key symptom in Zollinger-Ellison syndrome.

Complications of Gastric vs. Duodenal Ulcers

Bleeding
  • Gastric Ulcer: Bleeding from the left gastric artery.
  • Duodenal Ulcer: Posterior duodenal ulcer bleeds from the gastroduodenal artery.
  • Management: Fluid resuscitation, upper GI endoscopy, and cauterization of the ulcer base.
Perforation
  • Gastric Ulcer:
    • Fluid leaks into the lesser sac via the foramen of Winslow, causing lesser sac peritonitis.
  • Duodenal Ulcer:
    • More common than gastric ulcer perforation.
    • Fluid accumulates in the greater sac, causing greater sac peritonitis.
    • Anterior duodenal ulcers are more prone to perforation.
  • Overall most common cause of peritonitis is a perforated duodenal ulver.
Penetration
  • Gastric Ulcer:
    • Slow acid erosion into the posterior wall, potentially damaging the pancreas and causing necrotizing pancreatitis.
Obstruction
  • Gastric Ulcer:
    • Pyloric stenosis due to pylorus spasm and reactive fibrotic changes, leading to "teapot stomach."

Image-Based Questions

Gas Under Diaphragm
  • Signifies a perforation with peritonitis. Also known as the "Moustache sign."
Reverse Moustache Sign
  • Seen in acute pulmonary edema due to prominent pulmonary veins.
Pneumomediastinum
  • Air around the heart, known as "continuous diaphragm sign."
  • Associated with Boerhaave syndrome (esophageal rupture).
Subcutaneous Emphysema
  • Air in the chest wall, often seen with chest trauma or Boerhaave syndrome.
Coffee Bean Sign
  • Seen in sigmoid volvulus.
Birdbeak Appearance
  • On barium enema, indicates sigmoid volvulus.
Key X-Ray Findings (Must Not Miss):
  • Pneumothorax
  • Pneumoperitoneum (gas under diaphragm)
  • Pneumomediastinum

Sigmoid Volvulus Case

Presentation
  • 60-year-old male with left iliac fossa pain and obstipation (inability to pass flatus).
Diagnosis
  • X-ray shows a large bubble obstruction (coffee bean sign).
Rotation
  • Sigmoid volvulus rotates anticlockwise; cecal volvulus rotates clockwise.
Management
  • Pass a flatus tube.
  • Fluid resuscitation.
  • Colonoscopic detorsion; unlike stomach volvulus, exploratory laparotomy is generally not needed.

Diverticulitis Case

Presentation
  • 60-year-old hardcore non-vegetarian with chronic constipation, severe left iliac fossa pain, and hematochezia (fresh blood in stool).
Diagnosis
  • Diverticulitis, a leading cause of lower GI bleeding.
Investigation
  • CT abdomen is the preferred test.
  • Barium enema is used for diverticulosis, not diverticulitis.

Premalignant Conditions in the GI Tract (Top to Bottom)

Oral Cavity
  • Oral Submucosal Fibrosis: Due to gutka or betel nut use.
  • Leukoplakia: White patches; more common.
  • Erythroplakia: Red patches.
  • Syphilitic Glossitis.
  • Oral Lichen Planus: Controversial; low chance of malignancy but considered premalignant.
Esophagus
  • Tylosis Palmaris: Hyperkeratosis of palms and soles linked to squamous cell carcinoma.
  • Achalasia (HL Asiocardia): Increased lower esophageal sphincter tone.
  • Barrett's Esophagus: Due to GERD.
  • Plummer-Vinson Syndrome (Patterson-Kelly Syndrome):
    • Esophageal web (post-cricoid dysphagia).
    • Iron deficiency anemia.
    • Koilonychia (spoon-shaped nails).
    • Note: Glossitis is mentioned in some pathology resources but not consistently in gastroenterology.
    • Koilocytes: HPV-infected cervical cells from the cervix.
    • Leukonychia: White nails in liver disease.
Stomach
  • Gastric Ulcer.
  • Type A Gastritis.
  • Ménétrier's Disease:
    • Foveolar cell proliferation, leading to achlorhydria.
    • Cerebriform appearance of stomach mucosa (enlarged rugosities).
    • Treatment: Monoclonal antibody cetuximab (not gastrectomy).
Small Intestine
  • Crohn's Disease (also in large intestine).
  • Cronkhite-Canada Syndrome: Sporadic hamartomatous polyps.
  • Piotr Sager Syndrome: Hamartomatous polyps with mucosal melanosis.
Large Intestine
  • Familial Adenomatous Polyposis (FAP): APC gene on chromosome 5.
    • More than 100 polyps in the colon.
    • Prophylactic colectomy is performed to prevent adenocarcinoma.
    • Inflammatory Bowel Disease.
Piotr-Jeghers Syndrome
  • Genetics: Autosomal dominant, chromosome 19, STK11 and LKB1 genes.
  • Arborizing Pattern: Polyps with a plant-like growth pattern.
  • Mucosal Melanosis: Spots around the lips and inner orifice (palmar creases and knuckles are NOT involved as they would be in cases of Addison's disease).
  • Manifestations: Hamartomatous polyps, mainly in the jejunum.
  • Cancer Development: Increased risk of stomach cancer, ovarian cancer, cervical cancer, and hepatobiliary cancer. The polyps in the jejunum may not turn malignant.
  • Pre-Malignancy: Plus/minus; the incidence of cancer in extra-intestinal sites is increased.
  • Compared to oral lichen planus and Piotr-Jeghers Syndrome: Both have a lower chance of turning premalignant.