Dyspepsia and peptic ulcer disease Flashcards

1
Q

what is dyspepsia?

A

constellation of symptoms

  • epigastric pain or burning
  • postprandial fullness (postprandial distress syndrome)
  • early satiety (postprandial distress syndrome)
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2
Q

what are the organs of the foregut? where do they cause pain?

A
oesophagus
stomach
duodenum
pancreas
gallbladder
Pain in the epigastric region
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3
Q

how common is dyspepsia?

A

affects 20-40% of people globally
More common in H.pylori infection and NSAID use
PPI = most commonly prescribed drug

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4
Q

what causes dyspepsia?

A
organic causes:
- peptic ulcer disease
- drugs (NSAIDs, COX2 inhibitors)
- gastric cancer
functional causes:
- idiopathic, NU dyspepsia = 75% of cases
- no evidence of culprit structural disease
- can be associated with IBS etc
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5
Q

why is history important in dyspepsia?

A

differentiate between dyspepsia and reflux

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6
Q

how is dyspepsia examined?

A

if uncomplicated = epigastric tenderness only
if complicated =
- cachexia
- mass
- evidence gastric outflow obstruction (crushing splash?)
- peritonism

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7
Q

how is dyspepsia managed?

A

Monitor for alarm features
If ALARM features present = urgent GI referral
If ALARM features abscent = lifestyle advice , check for H. pylori infection

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8
Q

what is functional dyspepsia?

A

Presence of dyspepsia symptoms with no evidence of structural disease that is likely to explain the symptoms
Complicated interaction between the gut and the brain

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9
Q

what are the symptoms of peptic ulcer disease?

A

pain predominant dyspepsia (to back)
often also nocturnal
aggravated or relieved by eating (duodenal aggrevated by eating)

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10
Q

is peptic ulcer disease acute or chronic?

A

chronic

relapsing and remitting

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11
Q

who is peptic ulcer disease more common in?

A

lower socioeconomic groups

family history

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12
Q

what is the most common cause of peptic ulcer disease?

A

H. pylori

NSAIDs cause most of the rest

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13
Q

what is H. pylori and how is it acquired?

A

gram -ve microaerophilic flagellated bacillus
oral-oral/faecal-oral spread
usually acquired in infancy

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14
Q

when do the consequences of H.pylori infection arise?

A

later in life

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15
Q

what are the possible consequences of H. pylori infection?

A
Majority = no pathology
20-40% = peptic ulcer disease
1% = gastric cancer adenocarcinoma and lymphoma)
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16
Q

what has been attributed to the lower prevalence of H.pylori in the developed world and in the young?

A

sanitation, housing, hygiene etc

17
Q

how is acid produced in the stomach?

A

food increases pH in stomach, stimulating G cels, releasing gastrin into the bloodstream which stimulated parietal cells to produce acid
When pH drops again this signal stops
Negative feedback system

18
Q

H. pylori signals the g cells to produce gastrin which causes an overproduction of acid by parietal cells = hyperacidic state = increased acid flowing into duodenum = gastric metaplasia, duodenum van get infected?

A

ability to produce acid is reduced > pH of stomach rises > G cells pump out lots of gastrin to try and compensate, this high gastrin as well as atrophy is thought to be gastric cancer risk factor

19
Q

how can you differentiate between a complicated and uncomplicated peptic ulcer?

A
uncomplicated = clear edges, yellow fuzzy centre
complicated = darker, dot in the middle indicates risk of bleeding, looks deeper, irregular edges
20
Q

what do NSAID induced ulcers look like?

A

skipping ulcers down the tract

21
Q

what are some physical signs of gastric problems?

A

acute gastritis = red inflamed ruggae
chronic gastritis = lots of little bumps
Atrophy = flat and featurless

22
Q

how is H.pyori infection diagnosed?

A
most commonly = faecal antigen testing (FAT)
urease breath test
gastric biopsy:
- urease test
- histology
- culture/sensitivity
serology (IgA antibodies)
23
Q

H.pylori decreases the pH of its environment, true or false?

A

false

increases the pH of its environment

24
Q

what does H.pylori look like histologically?

A

bacilli sitting on top of the epithelium

25
Q

how is peptic ulcer disease treated?

A
All get PPI
All are tested for H.pylori
- +ve = eradicate and confirm
- -ve = antisecretory therapy (PPI)
withdraw NSAIDs
lifestyle advice
Non H.pylori/non NSAID ulcer = nutrition and optimise comorbidities
rarely surgery
26
Q

what is first line for H. pylori?

A

Triple therapy
PPI + Amoxicillin 1g + Clarythromicin 500mg
OR
PPI + metronidazole 400mg + clarithromycin 250mg
2 week regimen
If still symptomatic - retest

27
Q

what are the possible complications of peptic ulcer disease?

A

anaemia
bleeding
perforation
gastric outlet/duodenal obstruction - fibrotic scar

28
Q

when is a duodenal ulcer follow up required?

A

only if ongoing symptoms

Not needed if uncomplicated

29
Q

when is gastric ulcer follow up required?

A

follow up endoscopy at 6-8 weeks

ensure healing and no malignancy

30
Q

what are the side effects of Hpylori triple therapy?

A

nausea

diarrhoea