Peptic Ulcer Disease (4.4) Flashcards

1
Q

What is peptic ulcer disease (PUD)?

A

PUD is a term used to describe a group of ulcerative disorders that occur in areas exposed to acid-pepsin secretions

>gastric ulcer

>duodenal ulcer

>gastric erosions

>duodenal erosions

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2
Q

What are some signs and symptoms of PUD

A
  • Pain described as burning or gnawing and constant
  • Stomach ulcer: pain worsen after eating; duodenal ulcer: pain relieved by food
  • Waking up at night with pain
  • Non specific Sx: bloating, belching, heartburn,nausea
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3
Q

What are some complications of PUD

A

GI bleeding

  • Insidious (+ve faecal occult blood test)
  • Sudden, severe and without warning (haematemesis, melaena, weakness, syncope, increased Urea)

Penetration into an adjacent organ

  • intense and persistent pain, radiating to other sites

Gastric outlet obstruction (2%)

  • bloating, fullness, large volume vomiting
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4
Q

What are some alarm symptoms of PUD?

A
  • Unintentional weight loss
  • Haematemesis (vomiting blood or coffee-grounds like material)
  • Melaena (black, tarry faeces)
  • Iron deficiency anaemia
  • Dysphagia & odynophagia
  • Persistent vomiting, large volume vomiting
  • On NSAIDs or warfarin
  • >55 years if Sx persist in spite of initial management
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5
Q

For PUD;

A) Who is the patient

B) What are the symptoms?

C) How frequent are the symptoms

D) Action taken?

E) Medications?

F) Allergies?

A

A)

Caution in patient >55 yo due to increased risk of pathological condition

B)

  • Location of pain

>Localised epigastric pain

>Pain relieved by food? (duodenal ulcer)

  • Nature of pain

>Pain that wakes patient up at night

  • Any alarm symptoms?

C)

Pain with remission and relapses

D)

  • Has patient taken any PPI?
  • Any relieve from PPI?

E)

  • Are they on any medication that could potentially cause or increase risk of PUD

F)

  • Any previous allergic reaction to medication?

Patient presenting with symptoms of PUD need to be referred for accurate diagnosis

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6
Q

What are some causes of PUD?

A

Helicobacter pylori infection

  • 95% of DU and 85% of GU are associated with H.pylori
  • No symptoms in most infected patient

Non-steroidal anti-inflammatory drugs (NSAIDS) (including low-dose aspirin)

  • 15% of GU and 5% of DU among chronic NSAID users

Zollinge-Ellison Snydrome (rare)

  • Malignant tumour on the pancreas or duodenum; overproduction of gastric and acid
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7
Q

When is H pylori screening indicated in individuals?

A
  • Past or present history of PUD
  • Uncomplicated non-ulcer dyspepsia
  • Users of NSAIDs (inc low dose aspirin)
  • Personal hx of gastric cancer
  • Close relatives with gastric cancer
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8
Q

How does diagnosis of H pylori infection occur?

A

Serology

  • Presence of H. pylori specific IgG antibodies
  • Inexpensive and widely available
  • Not suitable for monitoring post-eradication

Urea breath test

  • Uses principle of urea metabolism by H. pylori
  • Suitable for post-eradication test
  • Urease is not present in human cells, its detection means that a urease producing organism (H pylori) is present
  • Patient swallows a 13C-urea capsule
  • Capsule comes in contact with gastric mucosa
  • If urease is present, it splits the urea into CO2 and NH3. C02 is absorbed into the stomach lining & exhaled in the breath as labelled 14CO2
  • Breath samples are collected at a timed sequence of 6,12, 20 mins after ingestion of capsule
  • The breath samples are then analysed with a liquid scintillation counter for the level of radioactivity

Stool antigen test

  • Presence of H. pylori antigen in the stool

Stop PPIs at least 2 weeks before the test and antibacterial 4 weeks before the test for an accurate result

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9
Q

What is the aim of H pylori eradication? Provide the regimen used for eradication and why resistance might fail

A

Aim: speeds up ulcer healing and reduces the chance of recurrent ulcer

If penicillin allergy: use metronidazole 400mg bd instead of amoxicillin 1000mg bd

  • Not curative in all patients > confirm eradication four weeks after completing regimen
  • True re-infection in Australia is uncommon after successful eradication

Reasons why first-line eradication might fail:

  • Incomplete adherence: side effects, tablet burden, duration
  • Resistance: clarithromycin 6-8%, metronidazole 50%, Amoxycillin still low
  • Other issues: clarithromycin drug interaction
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10
Q

What is a alternative H pylori eradication regime

A
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11
Q

How do NSAIDs cause gastric mucosal damage?

A
  • Direct irritation of the gastric mucosa
  • Systemic inhibition of the protective mucosal prostaglandin synthesis

Endoscopically confirmed gastric and duodenal ulcers occur in 15-30% of chronic NSAIDs users

  • Risk is increased with presence of other risk factors
  • More common in those recently started on NSAIDs; greatest risk in first month
  • Peptic ulcers induced by NSAIDs are gastric, often silent, presenting with acute complications
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12
Q

What are some other medications that increase the risk of NSAID-induced ulcers?

A
  • Clopidrogel
  • Sertraline, citalopram, escitalopram, fluxoetine, fluvoxamine
  • Prednisolone
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13
Q

How to prevent NSAID induced PUD?

A

Minimize NSAID use

> Simple analgesics & non-pharmacological tx

If NSAID required

> Least toxic, lowest possible dose, shortest acting, use for as short a time as possible

For patients with a past history of ulcer disease: test and treat for H.pylori before starting NSAID use

>Helicobacter pylori infection + NSAID –> increases the risk of ulcer disease 60-fold and bleeding amount of 6-fold

Prophylaxis in patients with one or more risk factors

  • Standard dose PPI
  • Double dose H2 antagonists
  • Misoprostol (poorly tolerated)
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14
Q

Do Cox-2 selective NSAIDs reduce risk of PUD?

A

Celecoxib, etoricoxib, meloxicam, parecoxib

  • Selective Cox-2 inhibitors reduce BUT do not eliminate risk of PU
  • Cox-2 inhibitors + low dose aspirin = no risk reduction for an ulcer
  • Increased risk of cardiovascular events
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15
Q

How to manage NSAID induced ulcer?

A

Stop the NSAID (exclude low dose aspirin) to allow ulcer to heal

>Simple analgesic if analgesic required

  • Heat ulcer with a standard dose PPI for 8-12 weeks
  • Test and treat for H pylori after ulcer has healed
  • AVOID NSAIDs in the future if possible
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16
Q

What to do if NSAID is still required?

A
  • Choice of least toxic NSAID
  • Lowest effective dose
  • Concurrent use of PPI (Does not completely prevent ulcer recurrence but reduce risk)
  • Trial of a Cox-2 selective NSAIDs if not on aspirin
  • Assessment of concurrent meds (If possible withdraw those that increase risk of PUD)
17
Q

Use of low dose aspirin and PUD

A
  • Low dose aspirin commonly indicated as secondary prophylaxis for ischaemic cardiac event
  • Increased risk of PUD with long term use of low dose aspirin –> 1 in 10 chronic users will have an ulcer at endoscopy but have no symptoms
  • Risk markedly increased with H pylori infection, concurrent NSAID
  • Risk not reduced by enteric-coated aspirin
  • Prevention strategy

> Screen and treat H pylori in patient with prior ulcer disease before starting low dose aspirin

> Prophylaxis with a PPI reduces risk

  • Recurrent bleeding less likely with aspirin + PPI than switching to clopidogrel