U9C1 H.pylori Flashcards
What is a peptic ulcer?
break in the lining of the GI tract extending through to the muscularis mucosa of the bowel wall
Why is the duodenum prone to ulceration?
Duodenal ulcers are associated with high-acid secretion while proximal gastric ulcers are associated with a low-acid output. The duodenum does not have the same protective mechanisms as thestomach mucosa as it is thinner.
What are the pathological features of a duodenal ulcer?
- Most common location: lesser curvature, in the anthrum
- Often solitary
- Sharply demarcated, slightly elevated, erythematous and edematous.
- Size: usually small and circular (0.5 to 2 cm), but may be 3cm (giant ulcer)
- Usually single lesion within 2 cm of pylorus
- Margins well defined
- No heaped up edges
- May have large vessel with open lumen at ulcer base
- Fibrosis and shortening of duodenum
- Brown ulcer base (digested blood), no induration of margins of ulcer
- Abrupt lesions with normal adjacent mucosa
- No scarring or blood vessel thickening
- Gastric foveolar cell metaplasia and chronic duodenitis common
- Various villus abnormalities in proximal duodenum with active duodenitis
- Brunner gland hyperplasia
- Helicobacter pylorioften present
What are the classifications of a peptic ulcer?
Type I = along lesser curvature of stomach & incisura
Type II = gastric + duodenal
Type III = prepyloric
Type IV = gastrosophageal junction or proximal cardia
Type V = linked to NSAIDs or aspirin usage
What are the symptoms of a peptic ulcer?
How does magnesium trisilicate and aluminium hydroxide relieve symptoms?
Magnesium trisilicate (MgSi3O8) reacts slowly with HCl to produce magnesium chloride (MgCl2) and silicic acid (H4Si3O8), which in turn degrades to form a colloidal mixture of metasilicic acid (H2SiO3), silicon dioxide (SiO2) and water.
Aluminium hydroxide (Al(OH)3) reacts rapidly with HCl to produce aluminium chloride (AlCl3) and water. AlCl3 in turn reacts with phosphate ions in the GI tract to produce insoluble aluminium phosphate (AlPO4).
The combination of the two agents provide both immediate (Al(OH)3) and more prolonged (MgSi3O8) relief from acid indigestion. However, this relief is temporary as the agents do not alter acid secretion.
What medications should be avoided before the breath test?
Antacids- stop the adhesion of h.pylori onto mucosal lining which reduces bacterial load
PPIs- antibacterial effect
Antibiotics- kill bacteria
What is H.pylori?
Helicobacter pylori is a spiral-shaped Gram-negative bacterium involved in the development of gastritis, duodenal and gastric ulcers, and gastric cancer.
How does the breath test work?
The carbon-13 (13C)-urea breath test detects the presence ofH. pyloriin the patient’s stomach. On the day of the test, patients have a sample of exhaled breath collected for analysis of CO2. They then drink 200 mL of an acidic liquid (orange juice or a mixture of citric, malic and tartaric acids) followed by 50 mL of a solution of urea labelled with13C. H. pyloriproduces large quantities of urease, an enzyme that cleaves urea into ammonia and CO2. The ammonia neutralizes stomach acid (NH3+ HCl➔NH4Cl) and allows the bacterium to survive in the gastric mucosa; the CO2escapes into theoesophagusand will appear in exhaled breath. When the breath isanalysedagain after 30 min, any13C‑labelled CO2will be derived from the labelled urea, indicating urease activity in the stomach and therefore indicating the presence ofH. pylori.
What other tests than the breath test can diagnose infection?
What part of the stomach is most likely to be colonised in an infection?
The antrum as it is the least acidic
What are the virulence factors and route of infection of H.pylori?
CagA (Cytotoxin-associated gene A) and VacA (Vacuolating cytotoxin A) are proteins produced by the bacterium Helicobacter pylori, known for its role in gastric ulcers and stomach inflammation.
CagA is associated with increased virulence and is injected into host cells, leading to alterations in cellular functions. It plays a role in the development of peptic ulcers and gastric cancer.
VacA, on the other hand, induces the formation of vacuoles in host cells, affecting cellular integrity and immune response. VacA contributes to H. pylori’s ability to survive in the acidic environment of the stomach.
How does H.pylori infection lead to duodenal ulceration?
