Peptic Ulcer Disease Flashcards
HELICOBACTERIA PYLORI INFECTION AND PEPTIC ULCER DISEASE (PUD)
• Break in Superficial Epithelial cells penetrating down to Muscularis
Mucosa or either Stomach or Duodenum; Formation of a Fibrous
base and increased Inflammatory cells
o C/f Erosions – Superficial breaks in Mucosa alone
• Duodenal Ulcers mostly found in Duodenal cap; Surrounding
mucosa appears inflamed, Haemorrhagic or Friable (Duodenitis)
• Gastric Ulcers are mostly seen on lesser curve near Incisura, but
also throughout stomach
• Duodenal Ulcers classically improve with food, while Gastric Ulcers
worsen with food
• DUs affect 10% of adults; 2-3× more common than GU; Increasing
incidence in elderly especially women; Higher PUD prevalence in
developing countries due to H pylori infection, NSAID induced ulcers increasing in incidence in
developed world
Presentation of Peptic Ulcer Disease
• Recurrent, Burning Epigastric pain; Relationship of pain to food is not reliable for diagnosis;
Relieved by Antacids; Pain of DU classically occurs at night, sometimes worse when hungry
o Persistent/Severe pain suggests complications (e.g. Penetration into other organs)
o Back pain suggests penetrating posterior Ulcer; Severe Ulceration might be
asymptomatic prior to Acute Bleeding
• Nausea might accompany pain; Vomiting infrequent but relieves pain
• Anorexia and Weight Loss especially with GU
• Symptoms might relapse and remit spontaneously due to onset of Atrophic Gastritis and
decrease in acid secretion
Helicobacter pylori Infection
• Slow-growing Spiral Gram-negative Flagellate Urease-
producing Bacterium; Colonises mucous layer of Gastric
Antrum and areas of Gastric Metaplasia; Found in greatest
numbers in mucous layers of Gastric pits adhering to
Gastric Epithelium
o Protected by Juxtamucosal Mucous layer where it traps bicarbonate from Antral Cells
and Ammonia produced by Bacteria Urease
• 80-90% of developing world, 20-50% of developed countries; Socioeconomic prevalence;
Faecal-Oral or Oral-Oral infection; incidence increases with age
• Ulcers common when infecting strain produces Cytotoxic Associated Protein CagA and
Vacuolating Toxin VacA; Associated with greater IL-8 production and hence more pronounced
inflammation and immune response
• Infection results in Antral Gastritis, Peptic Ulcer Disease (GU and DU), Gastric Cancer
o Chronic Antral Gastritis leads to Hypergastrinaemia from antral G cells; Results in
increased acid output
• Other H pylori Related Diseases include Distal (Not Proximal) Gastric Adenocarcinoma, and
Gastric B Cell (MALT) Lymphoma (H pylori Gastritis shown to contain clonal B cells)
Diagnosis of H pylori Infection
• Serological – IgG (90% sens, 83% spec); Takes up to 1yr to fall 50% after Eradication
•
13C-Urea Breath Test – Quick and reliable, used as screening; Measurement of 13CO2 after 13C-
Urea ingestion; Higher specificity and sensitivity
o Stop taking Antibiotics 4 weeks prior and PPIs 2 weeks before test
• Stool Antigen Testing – Specific Immunoassay using Monoclonal Antibodies for qualitative
detection; Replacing Urea Breath Test
o Stop taking PPIs 2 weeks before test (Can continue H2-antagonists)
• Endoscopic Testing – Especially for older patients and patients with Alarm symptoms
o Rapid Urease/CLO Test (Urea substrate conversion of Ammonia changing pH change
visualised by colour; False negative if on PPI or Antibiotics; Stop PPI 2 weeks prior,
Stop Antibiotics and Bismuth Compounds 4 weeks prior)
o Histology – Giemsa stained Gastric Mucosa ± Immunohistochemical staining
o Culture – Useful for antibiotic sensitivity, especially in refractory patients
• Patients who are under 55 with Typical PUD symptoms testing positive for H pylori can
commence eradication therapy without further investigations
Eradication Therapy for H pylori Infection
• Successful in 90% of patients; Reinfection is very uncommon (1%) in developed countries;
Higher in developing countries due to poorer compliance or Metronidazole resistance due to
increased use in parasitic infections
• Metronidazole, Clarithromycin, Amoxicillin, Tetracycline and Bismuth most widely used;
Amoxicillin and Tetracycline resistance is low (unless in countries where it is available OTC)
o Quinolones (e.g. Ciprofloxacin) can be used as rescue therapy
o Administered as combination of Strong PPI with two Antibiotics – Recent evidence
advocates use of Bismuth due to increasing Clarithromycin resistance
• PPI (E.g. Lansoprazole) with Clarithromycin, and either Amox or Metro for 1/52
o Prolonged PPI after triple therapy not necessary for ulcer healing, unless large or
complicated (haemorrhage, perforation) ulcer then continue till 4/52
• Simple DU/Infection can be assessed clinically; if symptoms persist, check eradication status
o Patients at risk of bleeding, or with complications, should always have Urea Breath
Test or Stool Antigen Test 6 weeks after end of treatment; Long term PPI might be
necessary if high likelihood of fatal rebleeding
• Patients with GU should be routinely re-endoscopied at 6 weeks to exclude Malignancy
Complication of Peptic Ulcer Disease
• Perforation – DU more common than GU; Usually into Peritoneal Cavity (via Lesser Sac);
Laparoscopic approach to close perforation and lavage; Conservatively managed by NG
suction, IV fluids and Antibiotics
• Gastric Outlet Obstruction – Prepyloric, Pyloric or Duodenal; Due to active Ulcer with
surrounding Oedema or Scarring after healing
o Differentials of Crohn’s disease or Pancreatic Carcinoma more common
o Distention of stomach leading to vomiting; Infrequent, Projectile, Large volume and
contains particles of previous meals
o Persistent vomiting causes loss of acid = Metabolic alkalosis; Settles with IV fluids and
Electrolyte replacement, NG suction and Acid Suppression
o Endoscopic Dilatation of Pylorus and Endoluminal stenting reduces need for surgery
• Surgery – Indicated only for Recurrent Uncontrolled Haemorrhage (Ligation of vessels) and
Perforation (Oversewing); Gastrectomy or Vagotomy no longer indicated
Postoperative Complications
• Recurrent Ulcer – Check for H pylori, Rule out Zollinger-Ellison Syndrome (Gastrinoma, usually
Pancreatic foci); Malignancy needs to be excluded in all cases
• Dumping – Upper Abdominal Symptoms (Nausea, Distention, Sweating, Presyncope,
Palpitations) following Gastrectomy and Gastroenterostomy; Due to rapid dumping of food
into Jejunum leading to rapid fluid shifts in plasma to dilute high osmotic load; Leads to
Hypovolaemia; Hypoglycaemia can also occur
• Diarrhoea – Seen after Vagotomy; Treatment with Antidiarrhoeal medication
• Nutritional Complications – Iron Deficiency (Malabsorption), Folate Deficiency (↓Intake),
Vitamin B12 deficiency (↓Intrinsic Factor), Weight loss (↓Intake)
NSAIDs, Helicobacter and PUD
• NSAIDs deplete Mucosal Prostaglandins (Inhibition of COX1) leading to mucosal damage; 50%
of patients on NSAIDs develop Gastric Mucosal Damage; 30% have Ulcers on Endoscopy; Only
small proportion symptomatic and 1-2% with major complications (e.g. GI Bleed)
• Large number on NSAIDs e.g. Low Dose Aspirin; Significant problem especially in Elderly
• H pylori and NSAIDs are independent and synergistic for PUD; 60× compared to control
• NSAIDs should be stopped and PPI given; H pylori Eradication if positive; If stopping NSAIDs
not possible (e.g. Intractable pain), NSAID with low GI risk at lowest dose possible or COX2
inhibitors (CI: CVS risk)
