Upper Gastrointestinal Disease Flashcards
Structure of normal GI
Epithelium
Submucosa
Muscularis propria
What is present in a normal oesophagus
Z line - squamo-columnar junction
Anatomy of the stomach
Oesphagus Cardia Fundus Body Pyloric antrum Pylorus Dueodenum
Normal stomach (body) histology
Lined by gastric mucosa, columnar epithelium (foveolar, mucin secreting)
Specialised glands in the lamina propria
Muscularis mucosa
Normal stomach (antral) histology
Lined by gastric mucosa, columnar epithelium (fovelolar, mucin secreting)
Non-specialised glands in the lamina propria (gastric pits)
Muscularis mucosa
Normal duodenum histology
Glandular epithelium with goblet cells (intestinal type epithelium)
Villous architecture with a villous:crypt ratio of >2:1
Acute inflammation of the oesophagus
Oesophagitis
Chronic inflammation of the oesophagus
GORD
Barrett’s oesophagus
GORD
Gastro-oesophageal reflux disease
Commonest cause of oesophagitis
Reflux of acidic gastric contents
Causes:
Ulceration: necrotic slough, inflammatory exudate, granulation tissue
Fibrosis
Complications of GORD
Haemorrhage
Perforation
Strictures
Barrett’s oesophagus
Barrett’s oesophagus
Re-epithelialisation by metaplastic columnar epithelium usually with goblet cells (intestinal type epithelium)
AKA columnar lined oesophagus (CLO)
Metaplasia of the oesophagus
Glandular epithelium (intestinal type)
Dysplasia of the oesophagus
Changes showing some of the cytological and histological features of malignancy, but no invasion through the basement membrane
Adenocarcinoma of the oesophagus
Invasion through the basement membrane
Now the commonest type of oesophageal cancer
Change from GORD-Barrett’s-Cancer
Metaplasia - Dysplasia - Cancer
Squamous cell carcinoma of the oesophagus
Associated with alcohol and smoking
Mid/lower oesophagus
Invasion into the submucosa
Carconoma of the oesophagus
Poor prognosis
Diagnosis of a pre-invasive stage is very important
Cause of oesophageal varicies
Cirrhosis of the liver (i.e. increased portal hypertension)
Gastritis
Inflammation of the gastric mucosa
Acute gastritis: acute insult
Chronic gastritis: chronic/persistent insult
Causes of acute gastritis
Chemical: aspirin, NSAIDs, alcohol, corrosives
Infection: e.g. helicobacter pylori
Causes of chronic gastritis
H pylori associated
Chemicals (NSAIDs, bile reflux into the antrum)
Autoimmune (body, auto-antibodies e.g. antiparietal)
Presence of lymphocytes +/- neutrophils
Mucosal associated lymphoid tissue induction (MALT)
Helicobacter associated gastritis
Caused by H.pylori infection
Pattern: chronic gastritis +/- activity
Outcome: CLO-IM-dysplasia, adenocarcinoma, lymphoma (MALToma)
Helicobacter pylori and stomach cancer
Helicobacter infection is associated with an 8x increased risk of (non-cardia) gastric cancer
cag-A-positive H.pylori have a needle like appendage that injects toxin into intercellular junctions allowing the bacteria to attach more easily.
This strain is associated with more chronic inflammation.
Treatment of the infection with antibiotics drastically reduces the risk of cancer.
Other causes of gastritis
Infection: CMV, strongyloides (immunosuppression)
IBD: Crohn’s disease
Why is gastritis concerning
Chronic gastritis –> ULCER = intestinal metaplasia –> dysplasia –> cancer
What should be done to all stomach ulcers
All ulcers should be biopsied to exclude malignancy
Complications of gastric ulcers
Bleeding: anaemia, shock (massive haemorrhage)
Perforation: peritonitis
Intestinal metaplasia
As in the oesophagus
Intestinal metaplasia in gastric mucosa in response to long term damage
Increased cancer risk
Gastric epithelial dysplasia
Abnormal epithelial pattern of growth
Some of the cytological and histological features of malignancy are present, but no invasive through the basement membrane
Causes of gastric cancer
Host factors and genes
Bacterial virulence factors
Environmental factors
Environmental factors for gastric cancer
Smoking
Poor diet
Gastric cancer
High incidence in Japan, Chile, Italy, China, Portugal, Russia
More common in men
>95% of all malignant tumors in stomach are adenocarcinomas
Classification of stomach adenocarcinomas
Intestinal - well differentiated
Diffuse - poorly differentiated (linitis plastica), includes signet ring cell carcinoma
Gastric cancer subtypes
95% are adenocarcinomas
Rest are: squamous cell carcinoma, lymphoms (MALToma), gastrointestinal stromal tumour (GIST), neuroendocrine tumours
Prognosis for gastric cancer
Overall survival is 15%
Gastric MALToma/ lymphoma
Chronic inflammation: Chronic immune stimulation
B cell (marginal zone) lymphocytes
Treatment: If limited to the stomach and H.pylori is present then H.pylori eradication
What is present in a normal duodenum
Villi
Duodenitis, Duodenal Ulcer and H. pylori infection
Increased acid production in the stomach which spills over into duodenum
Chronic inflammation and gastric metaplasia with helicobacter infection.
Especially in antral stomach infection = +++++ACID which spills into the duodenum.
Duodenal ulcers
Duodenitis and duodenal ulcer: good correlation between endoscopy and biopsy pathology
Endoscopy findings with duodenal ulcers
Endoscopy “itis”: 73.5% progress to ulcer, mainly erosive duodenitis (biopsy – neutrophils)
Pathogens causing duodenal ulcers (except H.pylori)
Immunosuppressed CMV Cryptosporidiosis Giardia lamblia infection Whipple's disease - trophryma whippelii
Duodenal malabsorption
Partial villous atrophy
Histology: villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes (normal range <20 lymphocytes/100 enterocytes)
Coeliac disease
Diagnosis requires:
endomysial antibodies and tissue transglutaminase antibodies
Duodenal biopsies:
On gluten rich diet showing villous atrophy
Off gluten showing normal villi
There are other causes of malabsorption with similar histology e.g. tropical sprue
Duodenal MALToma/lymphoma
Patients with coeliac disease have an increased risk of GIT cancers
MALToma associated with Coeliac is
in the duodenum
T-cell origin: Enteropathy Associated T-cell Lymphoma
