116 - Acute gastritis Flashcards
How quickly does acute gastritis heal?
A few days, because of rapid cell turnover in stomach.
What is acute gastritis often a response to?
Most commonly an acute response to a chemical injury,
alcohol or drugs (NSAIDs, aspirin, iron tablets and other
drugs), stress, shock, burns, head injury, septicaemia,
staphylococcal food poisoning
How does acute gastritis arise?
Due to breakdown of gastric barrier directly or via
microcirculatory changes accompanying shock or sepsis.
Chronic superficial gastritis histology
No erosion of stomach wall
More severe outcome of gastritis
Release of inflammatory mediators results in
vasodilatation, oedema, haemorrhage and erosions -
acute haemorrhagic or erosive gastritis
How can head injury lead to gastritis?
Can stimulate gastric acid secretion by affecting brain
Erosive ulcer
Degradation of mucosa
Acute ulcer
Degradation of mucosa, muscularis mucosae
Chronic ulcer
Degradation until subserosa, with fibrosis.
Scarring prevents regeneration of mucosa.
Cushing ulcers
Gastric and duodenal ulcers in persons with intracranial
injury
Curling ulcers
Ulcers in proximal duodenum associated with severe
burns/trauma
Three main types of chronic gastritis
– Autoimmune
– Helicobacter-associated
– Chemical
Other types of chronic gastritis (less common)
– Granulomatous (EG: Crohn’s disease)
– Lymphocytic
– Eosinophilic etc.
Autoimmune gastritis aetiology
Immune mediated destruction of acid secreting tubules
followed by atrophy with consequent achlorhydria and
loss of intrinsic factor leading to pernicious anaemia
(B12 deficiency)
Autoimmune gastritis areas affected
Confined to the gastric corpus (body) mucosa with total
loss of parietal cells. Antrum spared.
Effect of autoimmune gastritis
Loss of acid and parietal cells causes hypergastrinaemia
which leads to linear and nodular ECL hyperplasia and
occasionally to carcinoidosis.
Acid-secreting tubules aren’t regenerated, but enterochromaffin cells and D cells proliferate.
Autoantibodies generated in autoimmune gastritis
Circulating autoantibodies to parietal cell membrane – H+/K+ ATPase (90%) and intrinsic factor (70%) and gastrin receptor (70%).
Absorption issue in autoimmune gastritis
IF-Ab is secreted into the gastric lumen and can
complex with vitamin B12 preventing its absorption via
receptors in the terminal ileum
What characterises histology of autoimmune gastritis?
Normal antrum.
Gastric body acid secreting mucosa atrophy.
Linear and nodular hyperplasia of enterochromaffin-like cells
Total atrophy of acid secreting tubules, replaced by intestinal and pyloric gland metaplasia accompanied by
chronic inflammation
How does chemical gastritis come about?
Reflux of bile and alkaline duodenal juice due to alteredantro-duodenal motility or gastro-jejunostomy.
Long-term use of Aspirin, NSAIDs have a similar effect
Effects of chemical gastritis
Direct mucosal injury - disruption of the mucus layer and gastric barrier, epithelial desquamation
Histology of chemical gastritis 1 2 3 4 5 6 7
There is compensatory foveolar hyperplasia
Elongation and tortuosity of gastric pits
Vasodilatation and oedema
Fibromuscular hyperplasia of the lamina propria
Only mild inflammatory cell infiltration.
- Erosions/ulceration may result.
- Intestinal metaplasia can occur
Colonisation factors of H pylori 1 2 3 4
Motility
Microaerophilic
Adhesins
Urease
Epidemiology of H pylori in Australia
More prevalent in later life (increase in prevalence after ~40 years)
Type of gastritis from H pylori
1
2
3
1) Neutrophilic gastritis (soluble antigens and chemoattractants, IL-8)
2) Infiltration with chronic inflammatory cells
3) IgM, IgG, IgA appear at about 4 weeks, but don’t offer protection
Histology of H pylori
1
2
1) Tend to cluster around epithelial tight juncitons
2) Acute foveolitis with clusters of intraepithelial neutrophils, pit abscess and mixed neutrophilic and lymphoplasmacytic infiltration of the lamina propria
Timeline of H pylori infection (serious) 1 2 3 4 5 6
1) Normal mucosa
2) Chronic gastritis
3) Atrophic gastritis
4) Intestinal metaplasia
5) Dysplasia
6) Adenocarcinoma
Cancer that can arise from H pylori infection
Marginal zone lymphoma (B cell)
Two main patters of H pylori gastritis
1) Antrum-dominant
2) Pan-gastritis
Antrum dominant gastritis 1 2 3 4 5
1) Chronic inflammation and polymorphs
2) Increased acid output
3) Gastric metaplasia in duodenum
4) Active chronic inflammation in duodenum
5) Duodenal ulcer can arise
Pan-gastritis 1 2 3 4 5 6
1) Chronic inflammation, polymorphs
2) Atrophy
3) Intestinal metaplasia
4) Reduced acid output
5) Normal duodenum
6) Gastric ulcer can arise
Antrum-dominant gastritis
1) Increased acid load
2) Leads to low duodenal pH
3) Leads to Gastric foveolar cell metaplasia of D1 mucosa
4) Colonisation of duodenum by H pylori
5) Active chronic duodenitis +/- erosion
6) Duodenal ulcer
Diseases associated with H pylori 1 2 3 4 5 a, b
• Peptic ulcer disease (lifetime risk 1 in 6)
• Gastric adenocarcinoma – lifetime risk related to prevalence
of HP associated atrophic gastritis (1.5%-UK to 19%-China)
• Gastric B-Cell Lymphoma of MALT
• Iron Deficiency Anaemia
• Atrophic gastritis
– Susceptibility to bacterial
gastroenteritis
– B12 deficiency
Where are peptic ulcers most common?
D1, antrum
Other sites of peptic ulcers
1
2
3
– Oesophagus at squamocolumnar junction
with gastric cardia or Barrett’s mucosa
– Gastro-enterostomy stoma -
anastomotic/stomal ulcer
– Meckel’s diverticulum – 25% have heterotopic
gastric mucosa and peptic ulceration occurs if
colonised by H. pylori
Four zones of chronic peptic ulcer floor
- Exudate of fibrin, neutrophils and necrotic debris.
- Narrow zone of fibrinoid necrosis
- Zone of cellular granulation tissue
- Zone of fibrosis including endarteritis and hypertrophied nerves
Complications of peptic ulcers 1 2 3 4
1) Perforate
2) Haemorrhage
3) Penetrate (erosion into an adjacent organ)
4) Stenosis (contraction of scar can stenose pyloric canal)
Where can peptic ulcers penetrate to?
Often into pancreas.
Potential cause of haemetemesis, melaena
Haemorrhaging peptic ulcer
