gastrooesophageal ulcers Flashcards
what can cause acute oesophagitis
infection in immunocompromised patients: herpes simplex, candida, cytomegalovirus
corrosives
what can cause chronic oesophagitis
- Tuberculosis
- Bullous pemphigoid and Epidermolysis bullosa
- Crohn’s disease
reflux oesophagitis
what can cause gastro-oesophageal reflux disease
alchohol and tobacco obesity caffeine hiatus hernia motility disorder
what are the features of reflux oesophagitis
Squamous epithelium damaged – Eosinophils epithelial infiltration – Basal cell hyperplasia – Chronic inflammation increased desquamation ulceration, fibrosis, stricture, obstruction
what is barret’s oesophagus
lower oesophagus becomes lined with columnar epithelium
– Intestinal METAPLASIA
– ?Role of gastric/biliary reflux
– ?Role of Helicobacter pylori
• Premalignant - risk of adenocarcinoma of
distal oesophagus 100x general population
metaplasia due to chronic acid reflux
what is acute gastritis
inflammation of the stomach lining
due to chemical injury (NSAIDs or alcohol) or H. pylori
what can cause chronic gastritis
H. pylori
autoimmune
chemical
what do H. pylori look like
Gram negative spiral-shaped or curved bacilli
how is H. pylori treated
double antibiotics and proton pump inhibitors
what are the histological features of H.pylori infection
neutrophil infiltration
lymphoid aggregates with plasma cells infiltrate lamina propria
atrophy, fibrosis, metaplasia, gastric ulcer and gastric cancer
increased gastric acid secretion
duodenal ulcers
what are the two distribution patterns
involvement of antrum and body
or just antrum
how can H. pylori gastritis be detected
faecal bacteria, urea breath test, biopsy, urease test
what is reflux gastritis
regurgitation of bile and alkaline duodenal secretion
loss of epithelial cells with compensatory hyperplasia of foveolae
defective pylorus and motility disorders
what is Autoimmune Chronic Gastritis
Autoimmune reaction to gastric parietal cells
– Loss of acid secretion (hypochlorhydria / achlorhydria)
– Loss of intrinsic factor
• Vitamin B12 deficiency
• Macrocytic anaemia (Pernicious anaemia)
• Associated with marked gastric atrophy and intestinal
metaplasia
• Increased risk of gastric cancer
• Serum antibodies to gastric parietal cells and intrinsic
factor
what can cause peptic ulceration
hyperacidity – H pylori gastritis – Duodenal reflux – NSAIDs – Smoking – Genetic factors – Zollinger-Ellison syndrome
leads to a breach in the mucosal lining of the alimentary tract as a result of acid and pepsin attack
what are the complication of peptic ulcers
– Haemorrhage – Penetration of adjacent organs e.g. pancreas – Perforation – Anaemia – Obstruction – Malignancy
what is duodenal ulcer almost always caused by
helicobacter gastritis
what can lead to acute peptic ulceration
acute gastritis
stress response e.g. after severe burns
a result of extreme hyperacidity
where do chronic peptic ulcers tend to occur
at mucosal junctions
what leads to chronic peptic ulcers
hyperacidity
mucosal defence defects
what are the normal mucosal defences
mucus bicarbonate barrier
surface epithelium
what damages the mucus bicarbonate barrier
biliary reflux where bile refluxes into the stomach
what damages the surface epithelium
NSAIDS
H. pylori
what are the effects of gastric injury
necrotic debris
inflammation
granulation tissue
fibrosis
what causes duodenal ulcers
• Increased acid production – More important than for gastric ulcer – Can be induced by H pylori • Reduced mucosal resistance – Gastric metaplasia occurs in response to hyperacidity – Then colonised by H pylori
what is the histologica appearance of gastric ulcers
• Usually small, sharply demarcated (punched out), defined structure, granulation tissue,
what are the complications of duodenal ulcers
• ‘Bleed, burst or block’
• Penetration of adjacent organs e.g. pancreas
• Malignant change: rare in gastric ulcer and ‘never’ in
duodenal ulcer
what immune cells are involved in reflux oesophagitis
eosinophils
what type of epithelia is found in barret’s oesophagus
columnar
is H. pylori gram neg or pos
negative bacilli
how is H. pylori spread
oral- oral, faecal-oral or environment
what are the features of antrum only H.pylori infection
increased gastric acid secretion
duodenal ulcer
what are the features of antrum and body H. pylori
Atrophy, fibrosis, intestinal metaplasia
• Associated with gastric ulcer and gastric cancer
what is the histological appearance of chemical gastritis
loss of epithelia with crypt hypertrophy
what disease involves an autoimmune reaction to gastric parietal cells
autoimmune chronic gastritis
what are the two features of autoimmune chronic gastritis
loss of acid secretion
loss of intrinsic factor
what are the features of pernicious anaemia
macrocytic anaemia
B12 is needed in order to make RBCs
what is the histological appearance of chronic autoimmune gastritis
gastric atrophy and intestinal
metaplasia
increased risk of stomach cancer
antiparietal and intrinsic factor antibodies
what blood group is more likely to get a gastric ulcer
A
what blood group is more likely to get a duodenal ulcer
O
what social group is most likely to get a duodenal ulcer
even distribution
what social group is most likely to get a stomach ulcer
5
which are more common out of stomach and duodenal ulcers
duodenal ulcers are 3 times more common
what acid levels predispose to a stomach ulcer
normal or low
what acid levels predispose to a duodenal ulcer
normal or high
how often is H. pylori found in gastric ulcers
about 70%
in duodenal ulcers almost always
What is Curling’s ulcer
complication of severe burns due to ischaemia and necrosis
what can cause acute gastric ulcers
acute gastritis
burns
hyperacidity e.g. gastrin secreting tumour
what pathology destroys the mucus bicarbonate barrier
biliary reflux
what are the histological features of ulcers
fibrosis
inflammation
granulation tissue
necrosis
how common is cancer after having an ulcer
rare - stomach
‘never’- duodenum
what could cause pernicious anaemia
autoimmune gastritis
due to anti parietal cell and anti intrinsic factor antibodies
glandular atrophy and intestinal metaplasia
what is the histology of an H.pylori infection
cytotoxins immune response atrophy intestinal metaplasia peptic ulceration
what is biliary reflux
bile goes into your stomach
