peptic ulcer disease and gastric carcinoma Flashcards
how is an ulcer different to an erosion
- penetrates the muscularis mucosae
- can be acute or chronic (fibrosis)
prevalence of gastric-duodenal ulcers and m:f ratio, blood group
10% population
M:F 5:1
blood group A+
what is more common gastric or duodenal ulcers
duodenal ulcers
pathophysiology of peptic ulcer disease
produced by imbalance of gastro-mucosal defence mechanisms vs secretions and hormone gastrin
causes of peptic ulcer disease and why
- NSAIDs deplete mucosal defence
- stress: burn, sepsis
- smoking: damage and delay healing
- H.pylori
- acid pepsin vs mucosal resistance
- zollinger ellison syndrome get excess gastrin
prevalence of H.pylori in gastric vs duodenal ulcers
gastric=70%
duodenal=90%
what type of bacteria is H.pylori
spiral shaped gram negative acidophilic bacterium with flagella
where is h.pylori prevalence highest
africa and south america
more on socio-economic status
mechanism by which H.pylori isnt destroyed
- oral transmission
- produces urease to break down urea to bicarbonate and ammonia which buffers the acid
- adhesions help it to attach onto epithelial cells
where does h.pylori prefer in the body and why
lives in stomach next to epithelium in the antrum where it is protected by stomach mucosa
4 cytotoxins it produces h.pylori
- vacuolating cytotoxin (vacA) induction apoptosis, disrupt epithelial junction & block t cell response
- cytotoxin assoc. genes (cagA) alteration of signalling pathway and alter tight junctions
- phospholipases
- LPS induce inflammatory response
4 mechanisms of injury in H.pylori
-HYPERGASTRINEMIA
negative feedback for gastrin is blocked
-Antral somatostatin is depleted and increased gastrin release
- HYPERACIDITIY occurs with mucosal damage
- DIRECT MUCOSAL INJURY; cytotoxins
- INFLAMMATORY RESPONSE- mediated by macrophages, neutrophil & T cell
dx of H.pylori 4
- breath test: H.pylori produces from urea: ammonium and bicarbonate
- antibody measurement
- stool HP antigen test
- urease CLO test: take a biopsy from mucosa and place urea on it and see if it goes yellow to red
Prognosis of untreated H.Pylori infection
1.chronic active gastritis: predominantly antrum
(increased risk of duodenal ulcers)
2.chronic active pangastritis with some atrophy ( increased risk of gastric ulcers)
3.Chronic atrophic pangastritis (cancer risk)
4.metaplasia of duodenum
5.MALT gastric marginal B cell lymphoma
6. NSAID induced gastropathy
How do NSAIDS cause mucosal damage
affect COX1 also which is the housekeeping protective prostaglandins that protect mucosa
- increase mucosal blood flow
- stimulate bicarb and mucus secretion
Risk factors for NSAID induced ulcers 8
- age >60 years (atrophic gastritis)
- phx of PUD
- phx of adverse event with NSAID
- concomitant steroid use
- high dose NSAID or multiple
- hereditary predisp
- o blood group
- smoking
typical symptoms NSAID peptic ulcer disease
-epigastric pain (relief by food)
-nausea
-fullness
-bloating
-hunger pain
-night pain
ALARM S
alarm symptoms of NSAID peptic ulcer disease
anaemia haematemesis mealena vomiting anorexia pain radiation
treatment of benign peptic ulcer disease
- stop smoking
- avoid aspirin and nsaid
- PPI or H2 blockers
h.pylori eradication therapy
omeprazole 20mg
amoxicillin 1gram
clarithromycin 500mg
all three one week
omeprazole
clarithromycin 500mg
metronidazole 400mg
if fails can use Tripotassium Dicitratobismuthate 120mg or tetracycline
H.pylori eradication side effects
diarrhoea can get c.diff colitis metronidazole= metallic taste, flush, vomit headaches rash
management for NSAID induced ulcers
- stop NSAID or use lower dose
- co give with PPI
- use COX2 specifc eg celecoxib
5types of gastric carcinomas
- gastric adenocarcinoma
- gastric lymphoma
- GISTs (mostly benign leiomyomas)
- carcinoid tumours
- gastrinomas
factors assoc. with gastric carcinoma
some animals have fun playing all day games
smoking alcohol HP FAP syndromes pernicious anaemia Blood group A Diet rich in nitrosamines or salty and spicy gastric adenomatous polyps
