GI tract Flashcards
GI tract lining is
Squamous epithelium
Glandular epithelium may exist in
Illness
Barrett’s Oesophagus
Change from squamous epithelium to glandular
Columnar lined lower oesophagus - CELLO
Metaplasia
Change in differentiation of a cell from one fully diff type to a different type
Stable structure
Stomach lined with glandular epithelium which produces mucins to protect against acidic substances
Acid reflux causes ulceration and damage to oesophageal wall
Base of oesophagus undergoes
Adaptive change to endothelium
Mucins newly produced to protect against acid reflux
Cause of acid reflux and therefore barrett’s and potentially oesophageal cancer (adenocarcinoma)
Obesity due to pressure forcing acid upwards
Process of oesophageal cancer
GO reflux
metaplastic oesophageal glandular epithelium
dysplastic
neoplastic
Squamous cell carcinoma
Thought to be caused by smoking and alcohol
Helicobacter gastritis
Mechanism
presentation
Lives within mucin
Induce inflammation in stomach
Attract neutrophil polymorphs from surrounding areas
Stomach ache
Ulcers
gastric cancer
factors
presentations
smoked, pickled foods
Linitus plastica
low survival due to late presentation
coeliac disease
gluten sensitive enteropathy blunted villi - villous atrophy crypt hyperplasia increased no lymphocytes immune reaction to gluten allergy body produces T cells which attack gluten
inflammatory bowel disease
Chronic idiopathic inflammatory bowel disease
Crohn’s disease and ulcerative colitis
Crohn’s
What is the inflammatory response
Patchy inflammation from anywhere from bowel to anus
Aphthous ulcers extending through bowel wall and sometimes into fatty tissue
Granulomas - inflammatory response
Crohn’s disease complications
Inflammation
Perforation
Malabsorption
Neoplasia
Ulcerative colitis
Continous condition in mucosa of colon
Cut off between normal and inflamed tissue is obvious
Ulceration in mucosa
Diverticular disease
Out pouchings in wall of sigmoid colon
Diverts bowel matter
Inflamed sections may become perforated
DD development
Small gaps in mucosa for vessel
Internal high pressure of bowel e.g low fibre
Pressure causes mucosa to push matter through holes
Can perforate once inflamed
Colorectal cancer
Who does it affect?
Older people
People with adenomas
Dysplastic epithelium
Growth in mucosa
May be associated with local benign adenomas
Incidence increasing but deaths reduced
Normal epithelium –> adenoma –> colorectal adenocarcinoma
Familial adenomatous polyposis
mechanism
Development of 1000s of polyps on surface of colon
APC protein gene is mutated - may be folded or absent
Beta catenin levels rise unmoderated
Beta catenin moves into nucleus binds to DNA and encourages switch on of specific genes which leads to epithelial proliferation and adenoma
HNPCC
Hereditary nonpolyposis colorectal cancer
DNA repair protein gene nonactive therefore protein not produced
Macroscopic features of colorectal cancer
Brown staining around islands
Microscopic features of colorectal cancer
Adenocarcinoma
Colorectal cancer - staging and prognosis
Gives pt idea of prognosis
resection coding
- R0 - tumour completely excised locally
- R1 - microscopic involvement of margin by tumour
- R2 - macroscopic involvement of margin by tumour
prognosis and circumferential resection margin (CRM)
- CRM +ve 20% 5 year survival with 85% risk of local recurrence
- CRM –ve 75% 5 year survival with 10% risk of local recurrence
Dukes’ stage and prognosis
- A 95% 5 year survival
- B 75% 5 year survival
- C 35% 5yearsurvival
- D 25% 5 year survival
further spread = worse prognosis
