peptic ulcer disease Flashcards
definition of peptic ulcer disease
ulceration of areas of the GIT
caused by exposure to gastric acid and pepsis
most common: gastric and duodenal
can occur in oesophagus and Meckle’s diverticulum
aetiology of peptic ulcer disease
imbalance between damaging action of acid and pepsin, and mucosal protective mechanisms
strong correlation with Helicobacter pylori infection - unclear mechanism
common - very strong association with H pylori (95% of duodenal, 70-80% of gastric), NSAIDs
gastric cancer
rare - Zollinger-Ellison syndrome, crohn’s, sarcoidosis, TB
epidemiology of peptic ulcer disease
common
annual incidence 1-4/1000
males
duodenal - 30s
gastric ulcers - 50s
H pylori acquired in childhood and prevalence is equivalent to age in years
duodenal ulcer 4fold more common than gastric ulcer
sx of peptic ulcer disease
epigastric abdo pain (relieved by antacids) - related to hunger, specific foods, time of day, fullness after meals
radiate to back
heartburn - retrosternal pain
if worse soon after eating - gastric ulcer
if worse several hrs after eating - duodenal ulcer
+- weight loss
may present with complications:
- haematemesis
- melaena
beware ALARM Symptoms
can be asx - found incidentally or with crisis eg bleed
signs of peptic ulcer disease
may be no physical findings
epigastric tenderness
signs of complications:
- anaemia
- succession splash in pyloric stenosis
Ix for peptic ulcer disease
bloods
endoscopy
rockall scoring
testing for H pylori
histology of biopsy - difficult to visualise H pylori so limited value
for duodenal - measure gastrin concentrations when off PPI if Zollinger-Ellison syndrome is suspected
barium studies
bloods for peptic ulcer disease
FBC - low Hb (anaemia)
amylase - exclude pancreatitis
UE
clotting screen - if GI bleeding
LFT
cross match if actively bleeding
secretin test - if Zollinger-Ellison syndrome is suspected
secretin test
done if suspicion of zollinger-ellison syndrome
IV secretin = rise in serum gastrin in zollinger-ellison pts, but not in controls
endoscopy for peptic ulcer disease
4 quadrant gastric ulcer biopsies - rule out malignancy
repeat after 6-8wks to confirm healing and exclude malignancy
duodenal ulcers dont need to be biopsied
refer all with dysphagia, or >55 with ALARM Sx or treatment refractory dyspepsia
Rockall scoring - peptic ulcer disease
for severity after a GI bleed
<3 = good prognosis
>8 = high risk of mortality
testing for H pylori non-invasive
13C-urea breath test - radio-labelled urea given by mouth and detection of 13C in the expired air
serology - IgG Ab against H pylori - confirms exposure but not eradication
stool ag test - campylobacter-like organism test - gastric biopsy plaed with substrate of urea and a pH indicator - if H pylori is present - ammonia is produced from the urea and there is a colour change from yellow to red
acute Mx of peptic ulcer disease
resus if perforated or bleeding (IV colloids/crystalloids), close monitoring of vital signs, procedding endoscopic or surgical treatment
if upper GI bleeding - IV PPI (eg omeprazole or pantoprazole) at presentation until cause is confirmed
if actively bleeding peptic ulcer, or ulcer with high risk stigmata (eg visible vessel or adherent clot) - continue IV PPI
switch to oral PPI if no rebleeding within 24hrs
Mx for peptic ulcer disease
acute
drugs to reduce acid - PPI eg lansoprazole, or H2 blockers eg ranitidine
endoscopy - haemostatsis by injection sclerotherapy, laser or electrocoagulation
surgery if perf, or ulcer-related bleeding cant be controlled
H pylori eradication, and breath test to check for eradication
lifestyle - reduce alcohol and tobacco
follow up gastric ulcer with endoscopy 6-8wk - if not healed repeat biopsy to check for cancer
if extensive or recurrent ulceratoon consider unusual cause eg ZE
H pylori eradication
triple therapy for 1-02wks
1 PPI (eg lanosoprazole) and 2 AB (eg amoxicillin + clarithromycin, or Metronidazole + tetracycline)
less chance of recurrance and complications (bleeding) than if there is no eradication
Mx of peptic ulcer disease not associated with H pylori
treat with PPI or H2 antagonists
stop NSAIDS (especially diclofenac),
use misoprostol (prostaglandin E1 analogue) if NSAID use is necessary
Mx for drug induced ulcers
stop drug
PPIs for treating and preventing GI ulcers and bleeding in pts on NSAIDs or antiplatelet drusg
misoprostol is an alternative with diff SE
if sx persist - re-endoscope, retest for H pylori, reconsider ddx
surgery
complications of peptic ulcer disease
rate of major complication is 1%/year including:
- heamorrhage (haematemesis, melaena, IDA)
- perforation
- obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis, strictures)
- malignancy
- reduced gastric outflow
- recurrent ulceration
prognosis of peptic ulcer disease
overall lifetime risk 10%
generally good Px becayse when associated by H pylori - can be treated by erradication
ALARM Symptoms for peptic ulcer disease
anaemia - IDA
Loss of weight
Anorexia
Recent onset/progressive sx
Melaena/haematemesis
Swallowing difficulty
RF for duodenal ulcer
H pylori - 90%
drugs - NSAIDs, steroids, SSRI
increased hastric acid secretion
increased hastric emptying - low duodenal pH
blood gp O
smoking
sx of duodenal ulcer
asymptomatic
epigastric pain - relieved by antacids
+- reduced weight
RF for gastic ulcers
H pylori - 80%
smoking
NSAIDs
reflux of duodenal contents
delayed gastric emptying
stress eg neurosurgery or burns - Cushing’s, or Curling’s ulcers
RF for gastritis
alcohol
NSAIDs
H pylori
reflux/hiatus hernia
atrophic gastritis
granulomas - Crohn’s, sarcoidosis
CMV
zollinger-ellsion syndrome
Menetrier’s disease
Sx of gastritis
epigastric pain
vomiting
Ix for gastritis
upper Gi endoscopy only of suspicious features
definition of gastritis
histological presence of gastric mucosal inflammation
what is zollinger ellison syndrome
tumour of the endocrine pancreas – increase in gastrin production
= widespread ulceration to 2nd part of duodenum.
Rare for peptic ulcer disease because normally duodenal alkaline neutralse acid
antrum predominant H pylori gastritis
live in stomach anf survive in brush border of the stomach
antrum predominant
gastric pathology - chronic inflammation and polymorph activity
increased acid output
duodenal pathology - gastric metaplasia, active chronic inflammation
peptic ulcer risk - distal gastric and duodenal ulcer – acid drip into duodenum -> gastric metaplasia - h pylori infect here = ulcer
pangastrictis peptic ulcer
gastric pathology - chronic inflammation, polymorph activity, atrophy, intestinal metaplasia
Decreased acid output – suppression of acid secretion
Associated with gastric ulcer and cancer
If ulcer in body or fundus of stomach need to be V concerned
association of H pylori with gastric cancer
pan-gastritis linked to development of gastric cancer
adenocarcinoma of corpus and antrum and MALT lymphoma
cure lymphoma by eradicating H pylori
causal relationship
endoscopy based invasive tests for H pylori
rapid urease test – helicobacter produce urease – gel with coloured urea – if break down it changes colour yellow-> red
direct microscopy
histology
culture
DNA probes/PCR
endoscopy of NSAID peptic ulcer
multiple small ulcers
