GASTRIC DISORDERS Flashcards
Erosion vs ulcer
- Erosion: loss of epithelial layer, extending into muscularis mucosa
- Ulcer: loss of mucosal layer, can extend into submucosa or muscular layer
- What is gastritis?
- What are the two main types?
- How are they different in terms of cell involvement?
- What are causes of each?
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
What do the following do to parietal cells in the stomach?
- ACh
- Histamine
- Prostaglandins
- ACh, histamine: stimulate acid production
- Prostaglandins: inhibit acid production
Why do NSAIDs cause acute gastritis? 2 points
what type of patient should you consider at risk of acute gastritis from NSAID use?
- Block prostaglandin production → increase acid production from parietal cells
- Prostaglandins normally promote mucus/HCO3 production → NSAIDs remove this protection
♦ CHRONIC NSAID USERS ♦
Why can alcohol cause acute gastritis?
Stimulates acid production
How does chemotherapy cause acute gastritis?
Inhibits epithelial cell replication, compromising protective stomach layer
What type of stomach pathology are burns patients at increased risk of? Explain why this happens
how can this risk be reduced?
Curling’s ulcer
- Fluid loss → Dehydration → hypotension to stomach → mucosal ischaemia, necrosis
Result: acute gastritis and ulcers
► patients should be given PPIs as prophylaxis
How would increased intracranial pressure cause a stomach ulcer? What is the name of this type of ulcer?
Increased ICP caused by tumour or haemorrhage → increased of vagal tone → ++ACh to stomach → acid production → gastritis/ulcers
What type of gastric ulcer is common in critically ill patients? How is this prevented? Explain why it’s caused
Stress ulcer
Shock, sepsis, trauma → decreased mucosal perfusion → loss of protective barrier of mucus/HCO3
Prophylactic therapy: PPI
- 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?
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 ♦
What is the most common cause of chronic gastritis?
Which part of the stomach does it predominantly affect?
H. pylori: gram-negative rod, can cause both acute and chronic gastritis
Antrum of stomach
How does H pylori live in the stomach environment?
how does this damage the stomach?
- Urease → hydrolyses urea to ammonium (alkaline)
- Stomach detects this → releases gastrin → increases acid
- Ammonium can form ammonium chloride → further stomach damage
What are the two malignancies associated with H pylori?
- Gastric adenocarcinoma
- MALT lymphoma (mucosa associated lymphoid tissue)
What is the percentage of treatment failure in H. pylori?
Around 20% – patients should be re-checked after eradication
Chronic gastritis increases the risk of Gastric adenocarcinoma. What is the metaplasia that occurs before this happens? What is a key pathology finding?
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
Where do the majority of peptic ulcers occur?
what are they almost always caused by?
- 90% proximal duodenum
- 10% antrum/lesser curvature of stomach
H pylori infection: causes 90% of ulcers in duodenum, 70% in stomach
Which condition should you consider in a patient that has multiple ulcers present in the proximal and distal duodenum and jejunum?
Zollinger-Ellison syndrome
Why does eating relieve duodenal ulcer pain?
Eating a meal stimulates bicarbonate secretion
Explain the significance of Brunner’s gland hypertrophy
Brunner glands secrete alkaline fluid composed of mucin → coats duodenal epithelium
Only found in duodenum → glands become hypertrophied in peptic ulcer disease
What is the risk of posterior duodenal ulcers? 2 key points
Gastroduodenal artery posterior to duodenum → bleed can occur if ulcer erodes
Pancreas posterior to duodenum → pancreatitis can occur if ulcer erodes
Which anatomical landmarks separates upper and lower GI bleeding?
_Ligament of Treitz (_AKA suspensory ligament: 2 muscular ended ligament from Right crus of diaphragm to duodenojejunal junction)
What is the most common location for gastric ulcer? What happens if this ruptures? Artery involved?
Lesser curvature
Rupture will cause bleeding from left gastric artery
What is the most concerning cause of a gastric ulcer? How does this change investigation when compared with duodenal ulcers?
Gastric adenocarcinoma → ulcers in stomach often biopsied
Why are proton pump inhibitors often given before considering OGD in people with dyspepsia symptoms?
Treat GORD, gastritis, ulcers
If symptoms improve once on PPI, you can consider the condition treated without having to do invasive investigation
Explain the investigations you would do for a patient presenting with dyspepsia over 55 years old versus a patient presenting at 30
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
