GI tract Flashcards
What is the oeseophagus made up of?
It is a 25cm muscular tube lined by squamous epithelium.
There is a sphincter at the upper end and the gastro-oesophageal junction at the lower end.
Bottom 1.5-2cm is below the diaphragm and lined by glandular (columnar) mucosa
Squamo columnar junction is around 40cm from the incisor teeth.
What is reflux oesophagitis?
Most common form is GORD - gastro oesophageal reflux disease.
It is caused by a reflux of gastric acid - gastro-oesophageal reflux
Or - bile - duodeno-gastric reflux
What are the risk factors for reflux oesophagitis?
- obesity
- hiatus hernia
- pregnancy
- smoking
- NSAID’s, aspirin
- spicy foods
Symptoms of reflux oesophagitis?
- heartburn
belching, bloading, cough - can mimic heart pain
What is a hiatus hernia?
Stomach slides into thorax cavity from abdominal cavity via diaphragmatic opening.
It is due to - increased intra-abdominal pressures and/or decreased diaphragm tone (age)
What does a hiatus hernia result in?
Less sphincter competence -> gastric acid regurgitation -> oesophagitis/GORD
What are the two types of hiatus hernia?
Sliding - lower oesophageal sphincter incompetence - regurgitation of acid -> reflux
Paraoesophageal - sphincter okay but can trap the stomach - the protruding portion can become strangled and ischaemic –> emergency
What is the histopathology of reflux oesophagitis?
Normally have a small basal cell layer in squamous epithelium but in reflux oesophagitis there is basal cell hyperplasia, elongation of papillae and increased cell desquamation.
In lamina propria - inflammatory cell infiltratration (neutrophils, eosinophils and lymphocytes)
What are the complications of reflux oesophagitis?
Ulceration - if severe
Haemorrhage - if ulcers are severe they expose blood vessels and bleed
Perforation
Benign structure (narrowing)
Barrett’s oesophagus
Erosive tooth wear
What is Barrett’s oesophagus?
Complication of chronic gastro-oesophageal reflux disease
Up to 10% of patients with reflux suffer
Upward extension of squamo-columnar junction affected
What is the histology of Barrett’s oesophagus?
At the squamocolumnar junction squamous mucosa is replaced by columnar mucosa with goblet cells.
What condition does Barrett’s oesophagus predipose to?
Adenocarcinoma - there is an increased risk of developing this due to the process of metaplasia. 30x greater than general pop.
What is recommended for patients with Barretts oeseophagus?
Regular endoscopic surveillance recommended for early detection of neoplasia.
What are the two histological types of oesophageal cancer?
Squamous cell carcinoma
Adenocarcinoma
What increases the risk of adenocarcinoma?
- industrialised countries
- male gender (7:1)
- Caucasian’s
- Barretts oesophagus
- Smoking
- radiation
Where is the location of adenocarcinoma?
Lower oesophagus
Macroscopic features of adenocarcinoma
- Plaque like
- Nodular
- Fungating
- Ulcerated
- Depressed
- Infiltrating
Microscopic features of adenocarcinoma
Malignant cells forming glandular structures infiltrating connective tissue
Where is the incidence of squamous cell carcinoma high?
- Iran
- China
- South Africa
Southern Brazil
What are the risk factors for squamous cell carcinoma?
- Tobacco and alcohol
- Nutrition
- Thermal injury (hot beverages)
- HPV
- Male
- Ethnicity (black)
Where is the location of SCC?
Middle to lower 1/3rd
What precedes SCC?
Squamous dysplasia - normal squamous epithelium to high grade squamous dysplasia
Dysplasia - neoplasia confined to epithelium
Have squamous nests - cells invading surrounding tissue
What is the aetiology of gastric adenocarcinoma?
Diet - smoked/cured meat or fish and pickled vegetables
H. pylori infection
1% hereditary
What are the histological subtypes of adenocarcinoma?
Scattered growth - diffuse type (signet ring cell carcinoma)
Non scattered growth - intestinal type (tubular adenocarcinoma)
What is coeliac disease?
Chronic immune mediated enteropathy
Ingesition of gluten containing cereals - wheat, rye or barley
Genetically predisposed individuals - prevalence 0.5-1%
Any age
What is the pathogenesis of coeliac disease?
Gluten broken down to gliadin -> which is resistant to further breakdown due to amino acid sequence
In specific individuals gliadin activates CD4 T cells
These cause local inflammation, stimulates B cells to produce anti-gliadin/anti TTG antibodies
Gliadin causes IL15 to be produced by the epithelium -> activation/proliferation of CD8+ IELs (intraepithelial lymphocytes)
These IEL’s are cytotoxic and kill enterocytes (gut cells)
What are the symptoms of coeliac disease?
Diarrhoea and abdominal pain
What are other disease associations with coeliac disease?
Dermatitis herpetiformis
Lymphocytic gastritis
Lymphocytis colitis
Enteropathy associated T cell lymphoma
Small intestinal adenocarcinoma - rare
What are the oral manifestations of coeliac disease?
Enamel defects
Recurrent aphthous stomatitis
Delayed tooth eruption
Risk of caries
Smaller teeth
Angular chelitis
Oral lichen planus
Salivary gland dysfunction
Glossitis
Burning tongue
Geographic tongue
How do you diagnose coeliac disease?
Serologic blood tests usually performed before biopsy
Sensitive tests:
IgA antibodies to tissue transglutaminase TTG
IgA or IgG antibodies to deaminated gliadin
Anti-endomysial antibodies - specfic but less sensitive
Tissue biopsy
What is the treatment of coeliac disease?
Gluten free diet