Dyspepsia Peptic ulcer disease- clinical Flashcards Preview

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Flashcards in Dyspepsia Peptic ulcer disease- clinical Deck (16)
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What are the rome III criteria for dyspepsia?

Epigastric pain or burning
Postprandial fullness
Early satiey


What are the two broad categories of dyspepsia?

Organic causes:
Peptic ulcer disease
Drugs (especially NSAIDs and COX2 inhibitors)
Gastric cancer

Function causes:
No evidence of culprit structural disease
Associated with other functional gut disorders (e.g. IBS)


What is it important to differentiate dyspepsia from?

GORD may preexist/ predominate


What are alarm features that accompany dyspepsia?

Evidence of GI blood loss
Persistent vomiting
Unexplained weight loss
Upper abdominal mass


If GORD predominates in dyspepsia, how should it be managed?



If dyspepsia is not managed as GORD, and there are no alarm features, how should it be initially managed?

By considering lifestyle changes, and Antacids/H2RA


If dyspepsia symptoms are recurrent or persistent after managing lifestyle and using antacids/H2RA, what should be done?

Patients should be tested for H pylori.
Positive test: eradicate H pylori
Negative test: If patient is 55 or over, refer to hospital specialist
If patient is under 55, manage as functional dyspepsia


Describe the pain in peptic ulcer disease

Dyspepsia, moves to back
Often nocturnal
Aggravated or relieved by eating


a) What percentage of peptic ulcer disease is caused by H pylori?
b) What causes most of the rest of peptic ulcer?
c) what is happening to the ration of NSAID: H pylori peptic ulcers?

a) Approx 90% of DU
Approx 60% of GU
b) use of NSAIDs or COX 2 inhibitors
c) it is rising


What are the 3 different outcomes of H pylori infection?

1. No clinical disease
2. An intense distal gastritis response which causes hypergastrinaemia, resulting in increase acid secretion.
3. There is a pan gastritis which results in gastric atrophy, and there is a reduction of acid secretion.


Describe the pathophysiology of duodenal ulcer caused by H pylori.

There is increased gastrin release.
There is increased acid secretion in the stomach due to increased parietal cell mass and no body gastritis.
There is then increased duodenal acid load, which leads to gastric metaplasia, H pylori colonisation and ulceration.


How can H pylori be diagnosed?

Gastric biopsy: urease test (CLO test)

Urease breath test
Faecal antigen test
Serology (IgA antibodies- not accurate with increasing patient age)


When should the urease breath test not be used?

Within 2 weeks of PPI treatment or within 4 weeks of antibiotic therapy


What is the treatment for peptic ulcer disease?

All should have antisecretory therapy (PPI)
All should be tested for H pylori
If H pylori is positive: eradicate and confirm
If H pylori is negative: antisecretory therapy
Withdraw NSAIDs
Non H pylori and non NSAID peptic ulcers: nutrition and optimise comorbidities
No firm dietary recommendations
Surgery- infrequent


What is the eradication therapy for H pylori?

Commonest therapy is triple therapy for 1 week:
PPI + amoxycillin 1g bd + clarithromycin 500mg bd
PPI + metronidazole 400mg bd + clarithromycin 250 mg bd

2 week regimens:
Higher eradication rates
Poorer compliance
quadruple therapy + culture directed therapy


What is the follow up for peptic ulcer disease?

uncomplicated DU requires no follow up
Only follow up if ongoing symptoms

follow up endoscopy at 6-8 weeks
Ensure healing and no malignancy

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