Dyspepsia and Peptic Ulcer Disease Flashcards

1
Q

What is dyspepsia?

A
Indigestion and it presents with a constellation of symptoms:
Epigastric pain/burning (epigastric pain syndrome)
Postprandial fullness (postprandial distress syndrome)
Early satiety (postprandial distress syndrome)
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2
Q

Associations with dyspepsia?

A

No consistent association with sex, age, socioeconomic status, smoking or alcohol

More common if H. pylori infected and if their is NSAID use

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3
Q

2 categories of dyspepsia causes?

A

Organic causes for 25% of cases:
Peptic ulcer disease
Drugs, e.g: NSAIDs, COX2 inhibitors
Gastric cancer

Functional causes, i.e: idiopathic, for 75% of cases:
Definition is the same but there is no evidence of a culprit disease
Assoc. with other function gut disorders, e.g: IBS

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4
Q

What must dyspepsia be differentiated from?

A

GORD (heartburn)

However, sometimes dyspepsia and GORD can co-exist

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5
Q

What are the symptoms in uncomplicated dyspepsia?

A

Epigastric tenderness only

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6
Q

What are the symptoms in complicated dyspepsia?

A

Cachexia

Epigastric mass

Evidence of gastric outflow obstruction, e.g: abdominal distension and succussion splash (heard with stethoscope in epigastrium when patient is shaken at the flanks)

Peritonism

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7
Q

Management of dyspepsia?

A

If alarm symptoms are present, refer to a hospital specialist to ensure there is no gastric cancer

In the absence of alarm symptoms:
Check for H. pylori and eradicate if infected; this will cure ulcer disease and remove risk of gastric cancer. If dyspepsia is still a problem, despite eradication, refer to specialist
If H. pylori negative, consider a referral to specialist (over 55 years) or manage as functional dyspepsia (below 55 years)

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8
Q

Criteria for functional dyspepsia diagnosis?

A
Presence of at least one of:
Bothersome post-prandial fullness
Early satiation
Epigastric pain
Epigastric burning

and

No evidence of structural disease (inc. at upper endoscopy) that is likely to explain the symptoms

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9
Q

Factors influencing functional dyspepsia?

A
Visceral hypersensitivity
Altered brain-gut interactions
Genetic factors
Psychosocial factors
Abnormal upper GI motor and reflex functions
Disrupted gut-immune interactions
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10
Q

Symptoms of peptic ulcer disease?

A
Common cause of organic dyspepsia:
Epigastric pain (to the back) that often wakens people at night (not the case with functional dyspepsia); it is either aggravated/relieved by eating

It may be a relapsing/remitting problem and an FH may be common; more common with lower socioeconomic status

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11
Q

Which ulcers tend to be aggravated by eating and which are relieved?

A

Gastric ulcer - often relieved by eating (dilutes acid)

Duodenal ulcer - often aggravated by eating, which stimulated entry of chyme into the duodenum

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12
Q

What are the causes of peptic ulcer disease?

A

H. pylori causes 90% of duodenal ulcers and 60% of gastric ulcers

NSAIDS, inc. COX1, CO2 and PGE

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13
Q

What is H. pylori?

A

Gram negative microaerophilic flagellated bacillus

It is acquired in infancy via oral-oral/faecal-oral spread, but the consequences of infection do not arise until later in life

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14
Q

Consequences of H. pylori infection?

A

No pathology
Peptic ulcer disease

Gastric cancer:
Almost all are non-cardia gastric adenocarcinomas
Low grade B-cell gastric lymphomas (MALToma)
However, may reduce gastric cardia adenocarcinoma and oesophageal adenocarcinoma

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15
Q

2 ways that H, pylori affects acid production?

A
  1. Increased acid production will normally cause gastric ulcers; but gastric mucosa can develop in the duodenum and H. pylori can colonise it, leading to duodenal ulcers
  2. Promotes gastric atrophy and a decrease in parietal cells; this decreases acid secretion and it is a risk factor for gastric cancer
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16
Q

Appearance of duodenal, NSAID induced ulcers?

A

Burn-like appearance

17
Q

Appearance of gastric atrophy?

A

Flat surface

18
Q

Appearance of acute, uncomplicated gastric ulcer?

A

Yellow base

Treatment would be PPIs and eradication of H. pylori

19
Q

Diagnosis of H. pylori infection?

A

Gastric biopsy - urease test, histology, culture/sensitivity

Urease breath test

FAT (Faecal Antigen Test) - used in Tayside

Serology (IgA antibodies) - not accurate with increasing patient age

CUBT (Carbon urea breath test)

20
Q

How does H. pylori increases pH of its environment?

A

H. pylori produces the enzyme urease, which produces ammonium bicarbonate (can be detected by tests)

21
Q

Treatment of peptic ulcer disease?

A

Anti-secretory therapy, e.g: PPIs
If H. pylori positive, eradicate and confirm

Withdraw NSAIDs
Alter lifestyle
For non-H. pylori/non-NSAID ulcers, optimise nutrition and co-morbidities

22
Q

Anti-secretory therapies available for PUD?

A

4 H2 receptor antagonists - cimetidine, ranitidine, famotidine and nizatidine

PPIs inc. omeprazole, etc - more effective and faster

23
Q

Treating H. pylori infection?

A

Triple therapy:
PPI + amoxicillin + clarithromycin is the most common, for 1 week

2 week regimes are slower
Dual therapy PPI +1 antibiotic not recommended
Quadruple therapy + culture-directed therapy for people with resistance or allergies

24
Q

Complications of peptic ulcer disease?

A

Anaemia
Bleeding
Perforation
Gastric blue/duodenal obstruction - fibrotic scar (stricture)

25
Q

Follow-up for duodenal and gastric ulcers?

A

Duodenal - uncomplicated requires no follow-up; only if ongoing symptoms

Gastric - follow-up endoscopy at 6-8 weeks to ensure healing and no malignancy