GASTRIC DISORDERS Flashcards

1
Q

Erosion vs ulcer

A
  • Erosion: loss of epithelial layer, extending into muscularis mucosa
  • Ulcer: loss of mucosal layer, can extend into submucosa or muscular layer
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2
Q
  • What is gastritis?
  • What are the two main types?
  • How are they different in terms of cell involvement?
  • What are causes of each?
A

Inflammation of gastric mucosa

  • Acute gastritis: mucosal damage from acid - neutrophils. Numerous causes
  • Chronic gastritis: lymphocytes, plasma cells, macrophages. 2 common causes: autoimmune, H. pylori
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3
Q

What do the following do to parietal cells in the stomach?

  • ACh
  • Histamine
  • Prostaglandins
A
  • ACh, histamine: stimulate acid production
  • Prostaglandins: inhibit acid production
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4
Q

Why do NSAIDs cause acute gastritis? 2 points

what type of patient should you consider at risk of acute gastritis from NSAID use?

A
  • Block prostaglandin production → increase acid production from parietal cells
  • Prostaglandins normally promote mucus/HCO3 production → NSAIDs remove this protection

♦ CHRONIC NSAID USERS ♦

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5
Q

Why can alcohol cause acute gastritis?

A

Stimulates acid production

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6
Q

How does chemotherapy cause acute gastritis?

A

Inhibits epithelial cell replication, compromising protective stomach layer

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7
Q

What type of stomach pathology are burns patients at increased risk of? Explain why this happens

how can this risk be reduced?

A

Curling’s ulcer

  • Fluid loss → Dehydration → hypotension to stomach → mucosal ischaemia, necrosis

Result: acute gastritis and ulcers

► patients should be given PPIs as prophylaxis

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8
Q

How would increased intracranial pressure cause a stomach ulcer? What is the name of this type of ulcer?

A

Increased ICP caused by tumour or haemorrhage → increased of vagal tone → ++ACh to stomach → acid production → gastritis/ulcers

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9
Q

What type of gastric ulcer is common in critically ill patients? How is this prevented? Explain why it’s caused

A

Stress ulcer

Shock, sepsis, trauma → decreased mucosal perfusion → loss of protective barrier of mucus/HCO3

Prophylactic therapy: PPI

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10
Q
  • What is another name for autoimmune gastritis?
  • What happens in this condition?
  • which two parts of the stomach does it affect specifically?
  • which serious condition is this associated with?
A

Pernicious anaemia

Autoimmune destruction of parietal cells → loss of intrinsic factor secretion

Causes chronic inflammation in the gastric body and fundus (this is where parietal cells are found)

Intrinsic factor necessary for B12 absorption in terminal ileum

♦ RISK: Gastric adenocarcinoma ♦

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11
Q

What is the most common cause of chronic gastritis?
Which part of the stomach does it predominantly affect?

A

H. pylori: gram-negative rod, can cause both acute and chronic gastritis

Antrum of stomach

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12
Q

How does H pylori live in the stomach environment?

how does this damage the stomach?

A
  • Urease → hydrolyses urea to ammonium (alkaline)
  • Stomach detects this → releases gastrin → increases acid
  • Ammonium can form ammonium chloride → further stomach damage
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13
Q

What are the two malignancies associated with H pylori?

A
  • Gastric adenocarcinoma
  • MALT lymphoma (mucosa associated lymphoid tissue)
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14
Q

What is the percentage of treatment failure in H. pylori?

A

Around 20% – patients should be re-checked after eradication

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15
Q

Chronic gastritis increases the risk of Gastric adenocarcinoma. What is the metaplasia that occurs before this happens? What is a key pathology finding?

A

Intestinal metaplasia stomach tissue changes to intestinal tissue

Key pathology: finding is goblet cells in stomach → there are no goblet cells in normal gastric epithelium

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16
Q

Where do the majority of peptic ulcers occur?

what are they almost always caused by?

A
  • 90% proximal duodenum
  • 10% antrum/lesser curvature of stomach

H pylori infection: causes 90% of ulcers in duodenum, 70% in stomach

17
Q

Which condition should you consider in a patient that has multiple ulcers present in the proximal and distal duodenum and jejunum?

A

Zollinger-Ellison syndrome

18
Q

Why does eating relieve duodenal ulcer pain?

A

Eating a meal stimulates bicarbonate secretion

19
Q

Explain the significance of Brunner’s gland hypertrophy

A

Brunner glands secrete alkaline fluid composed of mucin → coats duodenal epithelium

Only found in duodenum → glands become hypertrophied in peptic ulcer disease

20
Q

What is the risk of posterior duodenal ulcers? 2 key points

A

Gastroduodenal artery posterior to duodenum → bleed can occur if ulcer erodes

Pancreas posterior to duodenum → pancreatitis can occur if ulcer erodes

21
Q

Which anatomical landmarks separates upper and lower GI bleeding?

A

_Ligament of Treitz (_AKA suspensory ligament: 2 muscular ended ligament from Right crus of diaphragm to duodenojejunal junction)

22
Q

What is the most common location for gastric ulcer? What happens if this ruptures? Artery involved?

A

Lesser curvature

Rupture will cause bleeding from left gastric artery

23
Q

What is the most concerning cause of a gastric ulcer? How does this change investigation when compared with duodenal ulcers?

A

Gastric adenocarcinoma → ulcers in stomach often biopsied

24
Q

Why are proton pump inhibitors often given before considering OGD in people with dyspepsia symptoms?

A

Treat GORD, gastritis, ulcers

If symptoms improve once on PPI, you can consider the condition treated without having to do invasive investigation

25
Q

Explain the investigations you would do for a patient presenting with dyspepsia over 55 years old versus a patient presenting at 30

A

Most cases of dyspepsia are functional. Around 25% have organic cause

  • >55/alarm symptoms: refer for endoscopy
  • younger, no alarm symptoms: H pylori test. Treatment if positive or PPI if negative
  • if initial treatment fails → endoscopy