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
What is inflammatory bowel disease and what two main conditions encompass it?
Chronic inflammatory process within the bowel resulting from inappropriate mucosal immune cell activation, encompassing: Crohn’s disease and ulcerative colitis
What are the affected bowel regions of UC and Crohn’s?
UC - colon only
CD - ileum +/- colon (any region)
What is the mucosal surface like in UC and CD?
UC - granular, red with broad flat ulcers with mucosal islands called pseudo-polyps
CD - linear fissuring ulceration (cobblestoning)
What are the 3 types of ulcerative colitis depending on their distribution?
UC is continuous from the rectum and moves up the colon
Rectum only - proctitis
Rectum/sigmoid - distal colitis
All colon - pan-colitis
How is crohn’s disease distributed?
Skip lesions - areas are affected at different parts of the colon
Is there stricture (narrowing) in either UC or CD?
UC - rare
CD - yes
What is the bowel wall like in UC and CD?
UC - thinned
CD - thickened
Prevalence of anal lesions in UC and CD?
UC - 25%
CD - 75%
Is there fistulae in either CD or UC?
UC - no
CD - yes
Is there fat wrapping in UC and CD?
UC - no
CD - yes
Is there a presence of granulomas in either CD or UC?
UC - no
CD - yes (35-60%)
What type of inflammation in CD and UC?
UC - superficial (mucosal)
CD - deep (transmural and can affect the outside and way through)
What are the pseudo polyps like in UC and CD?
UC - marked
CD - mild/moderate
Type of ulceration in UC and CD?
UC - superficial/broad
CD - deep/fissuring
Is there lymphocyte reactions in UC and CD?
UC - moderate
CD - marked
Is there fibrosis in UC and CD?
UC - mild/no
CD - marked (thick wall)
Is there serosal inflammation in UC and CD?
UC - mild/no
CD - marked (fat wrapping)
Can fistulas form in UC and CD?
UC - no
CD - yes
What are the clinical features of ulcerative colitis?
- diarrhoea
- rectal bleeding
- abdo pain
- weight loss
- constipation
- anaemia
- anorexia
- clinical pattern - most commonly intermittent, chronic continuous disease is rare
What are the oral manifestations of ulcerative colitis?
- associated with disease severity -
Ulceration
Tongue coating
Halitosis
Pyostomatitis vegetans - multiple small pustules on oral mucosal surface (can be seen in Crohn’s disease)
What are the symptoms of Crohn’s disease?
- affects all levels of GIT from mouth to anus -
Diarrhoea
Colicky abdo pain
Palpable abdominal mass
Weight loss/failure to thrive
Anorexia
Fever
Peri-anal disease
Anaemia
What are the oral manifestations of Crohn’s disease?
- Diffuse labilal/buccal swelling
- cobblestoning
- mucosal tags
- deep linear ulcerations
- mucogingivitis
- granulomatous cheilitis
What are the complications in the bowel for both UC and CD?
UC - toxic megacolon
Haemorrhage
Strictures - rare
CD - toxic megacolon and perforation
- fistula
- stricture (common)
- haemorrhage
- short bowel syndrome (repeated resection) causes malabsorption
What are some complications that can arise from both conditions?
Ulcers
Erythema nodusum
Percholangitis
Iritis
Clubbing
Who is more at risk of malignancy in UC and CD?
UC and colonic CD
What are risk factors of colorectal cancer in inflammatory bowel disease?
Early age of onset
Pancolitis
Primary sclerosing cholangitis
Family history of CRC
Severity of inflammation (pseudopolyps)
Premalignant changes
What is a polyp?
Tissue mass that protrudes from a surface
In the colon a polyp is a projection of mucosa that protrudes into the bowel lumen - can be single or multiple (polypopsis)
What are examples of non-neoplastic polyps?
Inflammatory polpys, hamartomatous (juvenile), hamartomatous (Peutz-Jeghers) and hyperplastic
What are examples of neoplastic polyps?
Adenomas (sessile - flat), malignant
What are pseudopolyps?
Islands of retained mucosa following ulceration
What are hamartomatous polyps?
Non neoplastic tissue elements typical for the site of origin but abnormal in organisation
What are juvenile polyps?
May be genetic
SMAD4/BMPR1A genes
Increased risk of cancer
Sporadic (not inherited) no cancer risk
<3cm in rectal
What are Peutz-Jeghers polyps?
Multiple polyps in small intestine, stomach, colon
Positive family history
Increase cancer risk
Characteristic appearance (abourizing)
Mucocutaneous pigmentation in 95% - often the first sign before any GI symptoms
What are hyperplastic polyps?
Commonly in left colon
Often multiple <5mm
Very characteristic - shaggy, teeth like, serrated
What are adenomas?
Benign tumours of colonic glandular epithelium - polypoid but also flat
Precursor lesions of colorectal cancer >80%
25-35% population >50 years
Small prop progress to cancer (10-15 years)
Where are adenomas distributed?
Evenly distributed around colon, larger in recto sigmoid and caecum
What are adenomas defined by?
Presence of pre-malignant change - called dysplasia but not malignant at this stage
What factors contribute to colorectal cancer?
Diet - fibre, milk, calcium, fruit, veg, vitamin D decrease
Red processed meat, dietary fat and alcohol
What lifestyle factors contribute to colorectal cancer?
Activity, cigarettes, drinking, obesity and age
What drugs affect risk of colorectal cancer?
Aspirin, NSAID’s, statins, OCP decrease risk
What health conditions increase risk of colorectal cancer?
Diabetes and IBD
What is the probable predisposition to colorectal cancer?
Genetics
Increases with more first degree relatives
What are hereditary cancer syndromes?
5-10% of colorectal cancers
Familial adenomatous polyposis
Lynch syndrome
What is autosomal dominant CRC syndrome?
In 80% of familial adenomatous polyposis - mutation in adenomatous polyposis coli tumour suppressor gene develops >100 of adenomatous polyps in colon.
If left untreated -> 100% risk of colorectal cancer by 40 years
What are the oral manifestations with Gardner syndrome?
Osteoma
Odontome
Supernumerary teeth
What are the majority of CRC’s?
Simple adenomatous
What are symptoms of colorectal cancer?
Change in bowel habits - diarrhoea, constipation
Feeling that bowel does not empty completely (tenesmus)
Stools
Bright red or dark blood
Narrower or thinner than usual
Abdominal pain
Unexplained weight loss, tiredness or unexplained anaemia (iron deficiency)
