Peptic ulcer disease Flashcards

1
Q

What is dyspepsia

A

Non specific symptoms related to upper GI

May relate to food, bloating, umbilical discomfort

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2
Q

Alarm symptoms with dyspepsia

A
Anaemia
Loss of weight
Anorexia
Recent onset of progressive symptoms or hematemesis
Swallowing difficulty
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3
Q

Signs to elicit

A

Tender epigastrium
Abdominal mass
Supraclavicular nodes

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4
Q

Managing new dyspepsia

A

FBC
FOBT

> 55 years or ALARM->Upper GI endoscopy

Stop drugs causing dyspepsia (NSAIDS, nitrates, anticholinergic, TCAs, CCB)
Lifestyle changes-> weight loss, smoking cessation, raise bed, small regular meals. Avoid hot drinks, spicy foods, alcohol, citrus, chocolate and eating test for H. pylori ->if +ve Eradication therapy and review in 4 weeks. If no improvement->UBT->if eradicated, do upper GI endoscopy
If initially -ve H pylori-> PPI for 4 weeks, if not improved will have longer dose and can consider upper GI endoscopy

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5
Q

What is more common gastric ulcers or duodenal ulcers

A

Duodenal

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6
Q

Major risk factors for duodenal ulcers

A

H pylori+++
NSAIDs, aspirin, steroids

Minor->+gastric acid, +gastric emptying, blood group O and smoking

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7
Q

Clinical presentation of duodenal ulcer

A

Epigastric pain before meals, at night

Relieved by eating or drinking milk

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8
Q

If doing an upper GI endoscopy, should PPIs be stopped

A

Yes, 2 weeks before

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9
Q

In what age group do gastric ulcers typically occur

A

Elderly

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10
Q

Risk factors for gastric ulcers

A
H pylori
Smoking
NSAIDs
Reflux of duodenal contents
Delayed gastric emptying
Stress-->neurosurgery = Cushing's ulcer, or burns->curling's ulcer
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11
Q

Symptoms of gastric ulcer

A

May be asymptomatic

Epigastric pain related to meals, relieved with antacids +/= weight loss

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12
Q

What is done at upper GI endoscopy

A

Visualise
Multiple biopsies
Cytology

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13
Q

How long is PPI treatment for GU compared to DU

A

GU->8 weeks

DU->4 weeks

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14
Q

Differential diagnosis of dyspepsia

A
Non-ulcer dyspepsia
OsophagitisGORD
DU/GU
Gastric malognancy
Duodenitis
Gastritis
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15
Q

Pathogenesis of GU related to NSAID use, intracranial, stress ulcers

A

NSAIDs-> -ve prostaglandins which normaly +mucin production and +vascular perfusion, therefore these are reduced

Intracranial->+activity of vagal nuclei= +gastric acid

Stress ulcers->splanchnic vasoconstriction

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16
Q

Complications of gastric ulcers

A

Perforation
Obstruction
Bleeding

17
Q

How does obstruction occur in gastric ulcers

A

Most commonly in chronic
Edema and scarring
Puloric channel ulcers

May present as incapacitating crampy abdominal pain, rarely total obstruction/intractable vomiting