H. pylori and ulcers Flashcards
Percentage of world population with h.pylori infection
approx 50%
90% develop chronic inflam with persistent infection (gastritis)
15% will develop ulcers
Related to stomach carcinomas
H. pylori
Gram negative bacteria
Spiral shape and flagella make it motile
Live in low pH of stomach
Transmission is fecal-oral and oral-oral
How does it metabolise urea
Has urease enzyme which breaks down urea in stomach.
forms a buuble of ammonia, which is alkali, allowing it to live in acidic conditions.
likes the ANTRUM as lower pH
Mechanism for h.pylroi infection
Can burrow thorugh mucosal layer in antrum, causing inflammation
Inhibits somatostatin release by damaging endocrine cells D cells
(somatostatin inhibits acid secretion by acting on G cells, ECL, parietal)
Therefore ACID SECRETION INCREASE
Molecules on h.pylori
Has sugar bining adhesion molecules Saba and Baba genes (Leb and sialyl-lex, which these bind to, are present in mucus and epithelial cs)
Also has cagA and vacA genes
cagA gene
Type IV secretion system
Disables epithelial tight junctions
Nod1 receptor recognises components of cell wall broken down and stimulates proinflam cytokine, causing gastric inflammation
vacA gene
A cytotoxin
forms large vacuoles
MUC5AC defence against H.pylori
Has glycoproteins Leb and sialyl-lex which h.pylori has sugar adhesins for. So h.pylori binds and gets stuck in this outer layer
MUC6 defence against h.pylori
If it gets through, MUC6 has different set of sugars, a 1-4 GlcNAc) which interferes with cell wall synthesis of h.pylori
MUC1 defence against h.pylori
If it gets past MUC6, then h.pylori will bind to the Leb and sialy-lex on MUC1
MUC1 will then be shed from the cell surface
Diagnosis for H.pylori
non invasive tests
Noninvasive
- Serological tests for IgG antibodies
- 13C- urea breathing test
- stool antigen test
Diagnosis for H.pylori
invasive
Require upper GI endoscopy and analysis of gastric biopsy
- biopsy urea test
- culture and histology
Treating h.pylori infection
2 antibiotics (amoxicillin and clarithromycin) 1 acid secretion decreasor (HPPI or H2 antagonist)
IF the triple cocktail doesnt work (sucessful in 90%) then can give bismuth chelate which lines the stomach
Causes of peptic ulcer disease
hyperacidity h.pyloi infection reflux of duodenal contents NSAIDs smoking (impairs mucus healing) Genetics (blood O and 1degree relatives) Males are 3 times more likely
Types of PUD
Duodenal
Gastric (especially at junction of antrum and body)
Duodenal ulcers
2-3 more common than gastric 15% of the population 90% of DU associated w h.pylori Epigastric pain is relieved by food, exacerbated by hunger Pain wakes them up at night Vomiting infrequent but can relieve pain Symptoms relapse and remit spontaneously
Gastric ulcers
70% associated w h.pylori, the rest with NSAID use
Linked to Zollinger-Ellison syndrome
Epigastric pain associated with food intake
Zollinger-Ellison syndrome
gastrin secreting pancreatic tumours that cause excess acid production, leading to acute ulcers
Treatment of PUD
PPI for at least 2 months
Treatment for h.pylori if necessary
Complications of PUD
- bleeding (most common)
- perforation, leading to peitonitis
- penetration into underlying tissue
- stricture, causig pyloric stenosis
- malignant change
Perforation of ulcer
Contents of stomach enter peitoneal cavity
most common in DU
Clinical signs of perforation
- Initial sudden, severe pain in upper abdomen that spreads (as gastric contents spead)
- shoulder tip pain due to diaphragm irritation
- shallow resp
- abdomen immobile (boardlike rigidity)
- bowel sounds absent
- after some hours sympotms may improve, but abdo rigidity remains.
- Later again deteriorates as peritonitis develops
Treatment for perforation
Surgery to oversew
What is dyspepsia
‘Indigestion’
upper abso symptoms like heartburn, acidity, pain, wind, fullness
