Lecture 4.2: Peptic Ulcer Disease Flashcards

1
Q

What is Peptic Ulcer Disease?

A

A disease when open sores that develop on the inside lining of your stomach and the upper portion of your small intestine

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2
Q

What are Symptoms of Peptic Ulcer Disease? (5)

A
  • Burning stomach pain
  • Feeling of fullness, bloating or belching
  • Intolerance to fatty foods
  • Heartburn
  • Nausea
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3
Q

What is GORD?

A

Gastro-oesophageal reflux disease (GORD) is a common condition, where acid from the stomach leaks up into the oesophagus (gullet)

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4
Q

What are Symptoms of GORD? (7)

A
  • Heartburn
  • Acid Reflux
  • Oesophagitis
  • Bad Breath
  • Bloating and Belching
  • Nausea
  • Vomiting
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5
Q

What is Barrett’s Oesophagus?

A

A medical condition where some of the cells in your oesophagus grow abnormally
If you have Barrett’s oesophagus you are slightly more likely to get oesophageal cancer

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6
Q

What is Gastritis?

A

Gastritis is inflammation of the gastric mucosa

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7
Q

What are Symptoms of Gastritis? (8)

A
  • Tummy Pain
  • Indigestion
  • Feeling full and bloated
  • Loss of appetite
  • Feeling sick (nausea)
  • Being sick (vomiting)
  • Not feeling as hungry as usual
  • Burping and farting
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8
Q

What is Dyspepsia?

A

Indigestion

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9
Q

3 Stages of Ulcer Formation

A

Fissure
Erosion
Ulcer

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10
Q

Causes of Gastritis (4)

A
  • Helicobacter pylori
  • NSAIDs (aspirin, ibuprofen)
  • Excess alcohol
  • Stressed/unwell
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11
Q

Characteristics of Helicobacter Pylori (7)

A
  • Motile, Flagellated
  • Gram Negative
  • Spiral/Helical Shape/Microaerophilic
  • Urease Producing
  • Adheres to gastric mucosa
  • Cytotoxin production
  • Transmissible
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12
Q

How does Helicobacter Pylori cause damage to the gastric mucosa? (6)

A
  • It secretes urease (this neutralised stomach acid)
  • Urease breaks down into ammonia and CO2
  • Ammonia, proteases and flagella help bacteria to
    invade the gastric mucosa
  • Thinning of mucosal layer due to damage
  • Epithelium destroyed
  • Ulcer formation
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13
Q

What does H.pylori produce that causes inflammation and is potentially a carcinogen?

A

Cytotoxin associated gene CagA

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14
Q

What does colonisation of predominately the antrum
by Helicobacter infection increase risk of?

A

Duodenal ulcer risk

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15
Q

What does colonisation of the antrum and body by Helicobacter infection increase risk of?

A

Largely asymptomatic

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16
Q

What does colonisation of predominately the body
by Helicobacter infection increase risk of? (3)

A
  • Gastritis
  • Gastric Ulcer
  • Cancer Risk
17
Q

Why does H. Pylori colonise different areas in different people?

A
  • In people producing large amounts of acid, it colonises
    nearer to the pyloric antrum to avoid the acid-
    secreting parietal cells at the fundus
  • In people producing normal or reduced amounts it can
    also colonises the rest of the stomach
18
Q

The inflammatory response caused by bacteria colonising near the pyloric antrum induces G cells in the antrum to secrete…?

A
  • Gastrin
  • Which travels through the blood downstream to the
    parietal cells in the fundus
19
Q

How common is H. Pylori?

A

At least half the world’s population is infected by the bacterium, making it the most widespread infection in the world

20
Q

What percentage of duodenal ulcers are associated with H.pylori?

A

About 95%

21
Q

What percentage of gastric ulcers are associated with H.pylori?

A

About 80%

22
Q

Causes of PUD (5)

A
  • H.Pylori
  • NSAIDs
  • Zollinger Ellison Syndrome
  • Smoking
  • Alcohol
23
Q

How can NSAIDs cause PUD?

A
  • The gastric mucosa protects itself from gastric acid
    with a layer of mucus
  • The secretion of which is stimulated by certain
    prostaglandins
  • NSAIDs block the function of cyclooxygenase 1 (cox-1),
    which is essential to produce these prostaglandins
24
Q

Mechanism of Prostaglandins

A
  • Stimulate mucus & bicarbonate
  • Vasodialate nearby blood vessels
  • Increased blood flow
  • Increased epithelial cell growth
  • Which inhibit acid secretions
25
Q

Treatments for PUD (5)

A
  • Smoking cessation
  • Reduce alcohol intake
  • Stop or review use of NSAIDs
  • PPI/H2 receptor antagonists
  • Eradication of h-pylori
26
Q

Complications of PUD

A
  • Perforation presenting as an ‘acute abdomen’
  • Upper GI bleeds presenting as heamatemesis or
    malaen
27
Q

Symptoms suggestive of hypovolaemic shock (5)

A
  • Dizziness (especially postural)
  • Fainting
  • Cool & clammy, delayed CRT
  • Hypotension, tachycardia
  • Low JVP
28
Q

Endoscopic Management of Bleeding (5)

A
  • Injection Sclerotherapy
  • Diathermy
  • Variceal Ligation
  • Laser Therapy
  • Endoscopic Clipping