Dyspepsia and Peptic Ulcer Disease Flashcards
What is dyspepsia?
epigastric pain or burning (epigastric pain syndrome)
postprandial (after a meal) fullness (postprandial distress syndrome)
early satiety (postprandial distress syndrome)
Where does the foregut start and end?
starts at: cricopharyngeus
finishes at: the ampulla of Vater
What factors make you more susceptible to peptic ulcer disease?
more common if H pylori infected
more common if NSAID use (can cause breakdown of the gastric mucosa)
overlap with IBS/GORD
What are the causes of dyspepsia?
Organic causes - 25%
•peptic ulcer disease
•drugs (especially NSAIDs, COX2 inhibitors)
•gastric cancer
Functional (idiopathic, NU) dyspepsia - 75%
•Epigastric pain and burning, early satiation, postprandial fullness AND no evidence of culprit structural disease (OGD, other tests)
•associated with other functional gut disorders e.g. IBS
What are the clinical signs of dyspepsia?
if uncomplicated
- epigastric tenderness only
if complicated
- cachexia (weight loss)
- mass
- evidence gastric outflow obstruction (vomiting)
- peritonism – evidence of a gastric ulcer
What is the first investigation of dyspepsia?
check H.pylori status (then eradicate if positive)
Describe peptic ulcer disease?
common cause of organic dyspepsia
pain predominant dyspepsia (radiates to the back)
often also nocturnal
aggravated or relieved by eating
relapsing & remitting chronic illness
lower > higher socio-economic groups
family history common
What causes Peptic Ulcers?
H.pylori infection
Use of NSAIDs (COX1, COX2, PGE)
Describe H. pylori infection?
Acquired in infancy
G -ve microaerophilic flagellated bacillus
Oral-oral / faecal oral spread
Consequences of infection do not arise until later in life – middle age
What are the consequences of H. pylori infection?
- No pathology - the majority
- Peptic ulcer disease - 20-40%
•95% of duodenal ulcers
•75% of gastric ulcers - Gastric cancer - 1%
•almost all non-cardia gastric adenocarcinoma (40% reduction when H pylori eradicated)
•low grade B-cell gastric lymphomas (MALT-oma)
•possible reduction in gastric cardia adenocarcinoma and oesophageal adenocarcinoma
How can H. pylori cause a duodenal ulcer?
H. pylori stimulates G cells to secrete gastrin - hypergastric state
This increased production of parietal cells which increases acid secretion
This increases duodenal acid load which causes h.pylori colonisation and then ulceration
How can H. pylori cause gastric cancer?
H. pylori stimulates G cells to secrete gastrin, this increased secreted gastrin destroys parietal cells and so there is atrophy of the stomach
Cag A is a powerful cytotoxin associated with gene A
How is H. pylori diagnosed?
gastric biopsy: urease test, histology, culture/sensitivity
urease breath test
FAT (faecal antigen test) – most common
serology (IgA antibodies) - not accurate with increasing patient age
What is the treatment of peptic ulcer disease?
ALL given antisecretory therapy (Proton Pump Inhibitor) •ALL tested for presence of H pylori •H pylori +ve - eradicate and confirm •H pylori -ve - antisecretory therapy •withdraw NSAIDs •lifestyle (difficult) •non-HP/non-NSAID ulcers - nutrition and optimise comorbidities •no firm dietary recommendations •surgery - infrequent
Which PPIs are affective in peptic ulcer disease?
including omeprazole, esomeprazole, lansoprazole, dexlansoprazole, pantoprazole and rabeprazole
omeprazole20-40 mg/day for two weeks OR
For one week:
PPI + amoxycillin 1g bd + clarithromycin 500mg bd
PPI + metronidazole 400mg bd + clarithromycin 250mg bd
