116 - Acute gastritis

Question 1

How quickly does acute gastritis heal?

Answer 1

A few days, because of rapid cell turnover in stomach.

Question 2

What is acute gastritis often a response to?

Answer 2

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

Question 3

How does acute gastritis arise?

Answer 3

Due to breakdown of gastric barrier directly or via

microcirculatory changes accompanying shock or sepsis.

Question 4

Chronic superficial gastritis histology

Answer 4

No erosion of stomach wall

Question 5

More severe outcome of gastritis

Answer 5

Release of inflammatory mediators results in
vasodilatation, oedema, haemorrhage and erosions -
acute haemorrhagic or erosive gastritis

Question 6

How can head injury lead to gastritis?

Answer 6

Can stimulate gastric acid secretion by affecting brain

Question 7

Erosive ulcer

Answer 7

Degradation of mucosa

Question 8

Acute ulcer

Answer 8

Degradation of mucosa, muscularis mucosae

Question 9

Chronic ulcer

Answer 9

Degradation until subserosa, with fibrosis.

Scarring prevents regeneration of mucosa.

Question 10

Cushing ulcers

Answer 10

Gastric and duodenal ulcers in persons with intracranial

injury

Question 11

Curling ulcers

Answer 11

Ulcers in proximal duodenum associated with severe

burns/trauma

Question 12

Three main types of chronic gastritis

Answer 12

– Autoimmune
– Helicobacter-associated
– Chemical

Question 13

Other types of chronic gastritis (less common)

Answer 13

– Granulomatous (EG: Crohn’s disease)
– Lymphocytic
– Eosinophilic etc.

Question 14

Autoimmune gastritis aetiology

Answer 14

Immune mediated destruction of acid secreting tubules
followed by atrophy with consequent achlorhydria and
loss of intrinsic factor leading to pernicious anaemia
(B12 deficiency)

Question 15

Autoimmune gastritis areas affected

Answer 15

Confined to the gastric corpus (body) mucosa with total

loss of parietal cells. Antrum spared.

Question 16

Effect of autoimmune gastritis

Answer 16

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.

Question 17

Autoantibodies generated in autoimmune gastritis

Answer 17

Circulating autoantibodies to parietal cell membrane –
H+/K+ ATPase (90%) and intrinsic factor (70%) and
gastrin receptor (70%).

Question 18

Absorption issue in autoimmune gastritis

Answer 18

IF-Ab is secreted into the gastric lumen and can
complex with vitamin B12 preventing its absorption via
receptors in the terminal ileum

Question 19

What characterises histology of autoimmune gastritis?

Answer 19

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

Question 20

How does chemical gastritis come about?

Answer 20

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

Question 21

Effects of chemical gastritis

Answer 21

Direct mucosal injury - disruption of the mucus layer and gastric barrier, epithelial desquamation

Question 22

Histology of chemical gastritis 
1
2
3
4
5
6
7

Answer 22

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

Question 23

Colonisation factors of H pylori
1
2
3
4

Answer 23

Motility
Microaerophilic
Adhesins
Urease

Question 24

Epidemiology of H pylori in Australia

Answer 24

More prevalent in later life (increase in prevalence after ~40 years)

Question 25

Type of gastritis from H pylori 1 2 3

Answer 25

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

Question 26

Histology of H pylori 1 2

Answer 26

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

Question 27

``` Timeline of H pylori infection (serious) 1 2 3 4 5 6 ```

Answer 27

1) Normal mucosa 2) Chronic gastritis 3) Atrophic gastritis 4) Intestinal metaplasia 5) Dysplasia 6) Adenocarcinoma

Question 28

Cancer that can arise from H pylori infection

Answer 28

Marginal zone lymphoma (B cell)

Question 29

Two main patters of H pylori gastritis

Answer 29

1) Antrum-dominant | 2) Pan-gastritis

Question 30

``` Antrum dominant gastritis 1 2 3 4 5 ```

Answer 30

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

Question 31

``` Pan-gastritis 1 2 3 4 5 6 ```

Answer 31

1) Chronic inflammation, polymorphs 2) Atrophy 3) Intestinal metaplasia 4) Reduced acid output 5) Normal duodenum 6) Gastric ulcer can arise

Question 32

Antrum-dominant gastritis

Answer 32

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

Question 33

``` Diseases associated with H pylori 1 2 3 4 5 a, b ```

Answer 33

• 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

Question 34

Where are peptic ulcers most common?

Answer 34

D1, antrum

Question 35

Other sites of peptic ulcers 1 2 3

Answer 35

– 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

Question 36

Four zones of chronic peptic ulcer floor

Answer 36

1. Exudate of fibrin, neutrophils and necrotic debris. 2. Narrow zone of fibrinoid necrosis 3. Zone of cellular granulation tissue 4. Zone of fibrosis including endarteritis and hypertrophied nerves

Question 37

``` Complications of peptic ulcers 1 2 3 4 ```

Answer 37

1) Perforate 2) Haemorrhage 3) Penetrate (erosion into an adjacent organ) 4) Stenosis (contraction of scar can stenose pyloric canal)

Question 38

Where can peptic ulcers penetrate to?

Answer 38

Often into pancreas.

Question 39

Potential cause of haemetemesis, melaena

Answer 39

Haemorrhaging peptic ulcer