Peptic ulcer disease and gastritis Flashcards
Define gastritis.
The histological presence of gastric mucosal inflammation. Usually dyspepsia which is not caused by an ulcer.
What are the 3 most common causes of gastritis?
- H pylori infection - non-erosive gastritis predisposing to atrophic gastritis and autoimmune gastritis
- NSAID use - acute erosive gastritis
- Alcohol - acute erosive gastritis
- Autoimmune e.g. pernicious anaemia
- Bacterial - phlegmonous gastritis due to staph aureus, strep, E coli, enterobacter etc.
What are the risk factors for gastritis?
- H pylori infection
- NSAID use
- Alcohol use/toxic ingestions
- Previous gastric surgery
- Critically ill patients
- AI disease -increased risk of AI gastritis in thyroid disease, idiopathic adrenocortical insufficiency, vitiligo, type 1 diabetes mellitus, and hypoparathyroidism.
Describe how NSAIDs cause gatritis.
NSAIDs inhibit prostaglandin production. This in turn decreases gastric mucosal blood flow with loss of the mucosal protective barrier
What is the pathophysiology of autoimmune gastritis?
Antiparietal cell antibodies cause immune infiltration and loss of parietal and chief cells in the gastric corpus
Describe the pathophysiology of phlegmonous gastritis.
Damage to the gastric mucosa may allow ingested bacteria to become invasive causing phlegmonous gastritis.
What are the signs and symptoms of gastritis?
Features are non-specific; check for presence of risk factors.
- Epigastric pain/dyspepsia
- Epigastric tenderness
- Vomiting, nausea, anorexia
No: features suggestive of malignancy e.g. anaemia, weight loss >10%, progressive dysphagia etc.
What investigations would you do for gastritis?
Urea breath test OR faecal antigen test- can be used first line if no features of malignancy and <60yrs; may be used to monitor therapy too.
Endoscopy +/- biopsy- 1st line if _>_60yrs or alarming features in younger patients. May show evidence of gastric erosions and/or atrophy +/- H pylori.
Other:
- FBC -may show low Hb and Hct and increased MCV in autoimmune gastritis; leucocytosis with left shift in phlegmonous gastritis
- Serum B12 (N or low in AI gastritis), parietal cell and IF antibodies (+ve in autoimmune gastritis)
- Intrinsic factor antibodies - highly specific for pernicious anaemia
- UGI contrast series - may show presence of gas which can confirm phlegmonous gastritis
How long should you withhold PPIs before non-invasive H pylori tests?
7-14 days
What is the management of gastritis?
Depends on type of gastritis:
H pylori - Eradication therapy - triple therapy/2Abx+PPI
- e.g. CAP: clarithromycin 500mg BD + amoxicillin 1g BD + omeprazole 20mg BD
Stress/erosive gastritis e.g. in ITU patients -
- Discontinue causative agents
- H₂ antagonists or PPI e.g. ranitidine/famotidine or pantoprazole
Autoimmune gastritis -
- B12/cyanocobalamin 1000mcg IM OM
Phlegmonous gastritis -
- ICU admission +
- Supportive care
- Broad spectrum Abx (ampicillin AND cirpofloxacin)
- +/- gastrectomy (but NG drainage and Abx should be sufficient)
What are the complications of gastritis?
- Gastric carcinoma/carcinoid/lymphoma
- Achlorhydria post atrophic gastritis (decreased/absent production of hydrochloric acid)
- Vit B12 deficiency
- Peptic ulcer disease → GI bleed
What is the prognosis with gastritis?
Erosive - symptoms improve after reduction of offending agent
Helicobacter pylori - initial triple therapy may sometimes be inadequate, so may require alternative quadruple bismuth-based regimen
AI gastritis - excellent prognosis with B12 treatment
Phlegmonous gastritis - mortality rate for surgically treated patients ~20% and for medically treated patients is ~50%
Describe the bacteria H.pylori. Where does it reside?
Gram negative, motile, microaerophilic bacterium
Resides in human GI tract – exclusively colonising gastric-type epithelium
It is a commensal
How do ulcers form?
- Increased gastric acid formation – through increased gastrin or decreased somatostatin production – this shifts the balance to more acid production
- Gastric metaplasia of epithelial cells– cell transformation due to excessive acid exposure
- Downregulation of defence factors - reduces epidermal growth factor & reduces bicarbonate production(which increases acidity)
What are the two virulence factors produced by H.pyroli and what responses does each cause?
- CagA -> antigenic response
- VacA -> cytotoxic response
What are the main virulent components of H pylori?
_Urease* enzyme production_ – (20% of the dry weight of this bacteria is the urease enzye) catalyses urea into ammonium chloride (which is toxic) & monochloramine–> damage epithelial cells
Urease is antigenic–> evokes immune response à damage to epithelial cells
Certain virulent strains produce CagA (antigenic) or VacA (cytotoxic) – more intense tissue inflammation
Describe the pathophysiology of a complicated peptic ulcer.
- Dissolves mucus layer: urease enzyme
- Causes epithelial cell death: exotoxins & inflammation
- Increased acidity –> peptic ulcer
Define peptic ulcer disease.
A break in the mucosal lining of the stomach or duodenum >5 mm diameter, with depth to the submucosa. Smaller ulcers are called erosions.
Usually gastric or duodenal due to exposure to gastric acid or pepsin.
Name 2 common and 1 rare cause of peptic ulcer disease.
Common:
- Hpylori (in 95% of duodenal and 70-80% of gastric ulcers),
- NSAID use
Rare: Zollinger-Ellison syndrome
How common is peptic ulcer disease?
- Duodenal > gastric
- H pylori causes 95% of duodenal ulcers and 75% of gastric ulcers
- Common - ~5% prevalence
- M>F
- Duodenal usually present in 30s
- Gastric usually present in 50s-70s
NB: H pylori is usually acquired in childhood and prevalence is roughly equivalent to the age in years.
What are the risk factors for PUD?
- Helicobacter pylori infection - present in >90% of patients with duodenal ulcer and >70% with gastric ulcer.
- NSAID use
- Smoking
- Increasing age
- Personal or family history of peptic ulcer disease
- An intensive care stay.
List 3 drugs which may cause or exacerbate dyspepsia.
- Alpha blockers
- Anticholinergics
- Aspirin
- Benzodiazepines
- Beta blockers
- Bisphosphonates
- CCB
- Corticosteroids
- Nitrates
- NSAIDs
- Theophyllines
- TCAs
What is a typical presentation of peptic ulcer disease?
Dyspepsia - commonly related to eating and experienced at night
Relieved by antacids
Discomfort
Chronic or recurrent nature
Pointing sign - patient can point to where the pain is exactly
Nausea, anorexia, and vomiting - uncommon, but if present may be relieved by eating.
Variable relationship to food:
- if worse after eating then more likely gastric
- if symptoms worse several hours after eating OR symptoms relieved by eating then duodenal
May present with complications e.g. haematemesis, melaena → urgent referral to secondary care
What investigations would you do for peptic ulcer disease?
Endoscopy is the gold standard diagnostic test but urea breath test or H pylori stool antigen test may be done instead if no suspicion of malignancy.
Bloods:
- FBC - anaemia
- Amylase - exclude pancreatitis
- U&Es, clotting screen (if GI bleeding)
- LFT
- Cross-match if actively bleeding
- Secretin test - If zollinger-Ellison suspected then IV secretin causes rise in gastrin in SE patients but not controls
Tests for H pylori
Endoscopy - 4 quadrants need to be sampled to rule out malignancy, duodenal ulcers need not be biopsied
