Pathology of the GI tract Flashcards
Describe the normal oesophagus
- Lined by squamous epithelium
- Distal 2cm below diaphragm lined by glandular columnar mucosa
- Cricopharyngeal sphincter & gastro-oesophageal junction
What layers make up the normal histology of the oesophagus?
- Mucosa (epithelium & lamina propria)
- Submucosa
- Muscularis propria
What is Oesophagitis?
- Inflammation of the oesophagus either acute or chronic
- Infectious=bacterial, viral (HSV1, CMV), fungal (candida)
- Chemical= reflux, ingestion of corrosive substance
What is reflux oesophagitis?
- Commonest form
- Caused by reflux of gastric (gastro-oesophageal reflux) acid &/or bile (duodeno-gastric reflux)
- Leading symptom= heartburn
What are the risk factors for reflux oesophagitis?
- Hiatus hernia
- Defective lower oesophageal sphincter
- Inc intra-abdominal pressure
- Inc gastric fluid vol due to gastric outflow stenosis
What are the types of hiatus hernia?
- Sliding hernina= reflux symptoms
- Paraoesophageal hernia= strangulation
What changes in histology will be seen in reflux oesophagitis?
- Squamous epithelium= basal cell hyperplasia, elongation of papillae, inc cell desquamation
- Lamina propria= inflammatory cell infiltration (neutrophils, eosinophils, lymphocytes)
What are complications of reflux oesophagitis?
- Ulceration
- Haemorrhage
- Perforation
- Benign stricture (segmental narrowing)
- Barrett’s oesophagus
Describe Barrett’s oesophagus
- Cause= longstanding reflux
- RF= male, Caucasian, overweight, same as for reflux
- Macroscopy= Proximal extension of squamo-columnar junction
- Histology= Squamous mucosa replaced by columnar mucosa- glandular metaplasia (same as stomach lining)
What types of columnar mucosa are there in Barrett’s oesophagus?
- Gastric cardia type
- Gastric body type
- Intestinal type= specialised Barrett’s mucosa
How and why is Barrett’s oesophagus monitored?
- Premalignant condition w/ inc risk of developing adenocarcinoma
- Regular endoscopic surveillance to detect early neoplasia
How does Barrett’s oesophagus progress into cancer?
1) Barrett’s oesophagus
2) Low-grade dysplasia
3) High-grade dysplasia
4) Adenocarcinoma
What are the 2 types of oesophageal carcinoma? Risk factors? Location? Macroscopy?
- Adenocarcinoma= tobacco, obesity, Barrett’s oesophagus, diet (smoked/cured/pickled meat or fish), H.Pylori, hypochlorhydria (allows bacterial growth) male, Caucasian. Lower oesophagus. Plaque-like, nodular, fungating, ulcerating, infiltrating, depressed.
- Squamous cell carcinoma= tobacco, alcohol, male, black, HPV, thermal injury-hot beverages, nutrition-nitrosamines. Middle & lower 3rd. Preceded by squamous dysplasia
What does the ‘T’ stand for in TNM staging?
- Depth of invasion of the primary tumour
- T1= tumour invades lamina propria, muscularis mucosae/submucosa
- T2= tumour invades muscularis propria
- T3= tumour invades adventitia
- T4= tumour invades adjacent structures
What does the ‘N’ stand for in TNM staging?
- Regional lymph nodes
- N0= no node mets
- N1= 1-2 node mets
- N2= 3-6 node mets
- N3= 7+ node mets
What does the ‘M’ stand for in TNM staging?
- Distant metastasis
- M0= no metastasis M1= distant metastasis
What are the 4 anatomical regions of the stomach? And the 3 histological regions with different functions?
Anatomic regions: Cardia, body, fundus, antrum
Histological regions: Cardia, body, antrum
What are the normal stomach defences?
- Balance of aggressive (acid) & defensive forces
- Surface mucosa
- Bicarbonate secretion
- Mucosal blood flow
- Prostaglandins
- Regenerative capacity
What things can lead to increased aggression (acid) in the stomach?
- Excessive alcohol
- Drugs
- Heavy smoking
- Corrosive/radiation/ chemotherapy
- Infection
What things can lead to impaired defences in the stomach?
- Ischaemia
- Shock
- Delayed emptying
- Duodenal reflux
- Impaired regulation of pepsin secretion
What can H. Pylori lead to?
- Damages epithelium leading to chronic inflammation of mucosa
- Results in glandular atrophy, replacement fibrosis & intestinal metaplasia
- More common in antrum than body
What are complications of H.Pylori?
- Corpus predominant: MALT lymphoma, Hypochlorhydira atrophy/intestinal metaplasia Gastric ulcer/cancer
- Antral predominant: Hypergastrinaemia Hyperchlorhydriapre-pyloric gastric ulcer or gastric metaplasiaduodenal ulcer
What is peptic ulcer disease? Where are the major sites and causes?
- Localised defect extending at least into submucosa
- 1st part of duodenum, GOJ, junction of antral & body mucosa
- Hyperacidity, H.Pylori infection, drugs(NSAIDs), smoking, duodeno-gastric reflux
Describe what an acute gastric ulcer would look like histologically
- Full thickness coagulative necrosis of mucosa
- Covered w/ulcer slough (necrotic debris, fibrin, neutrophils)
- Granulation tissue at ulcer floor
Describe what a chronic gastric ulcer would look like histologically
- Clear-cut edges overhanging at base
- Extensive granulation & scar tissue at ulcer floor
- Scarring often throughout entire gastric wall breaching muscularis propria
- Bleeding
What are complications of peptic ulcers?
- Haemorrhage (acute or chronicanaemia)
- Perforationperitonitis
- Penetration into adjacent organ (liver, pancreas)
- Stricturing (hour glass deformity)
What are differences between gastric and duodenal ulcers?
D: inc up to 35yrs, acid levels are elevated/normal, 95% H.pylori, located at bulbus, mainly blood group O
G: inc with age, acid levels normal/low, 70% H.Pylori, located at lesser curve, antrum-corpus junction, prepyloric, mainly blood group A
What are the most/less frequent gastric cancers?
Most= adenocarcinoma Less= MALT lymphomas, stromal tumours (GIST), endocrine tumours
What does a carcinoma of the GOJ or body/antrum show?
GOJ: white males, association w/GO reflux NOT H.Pylori/diet
B/A: Associated w/ H.Pylori, diet/salt NOT GO reflux
Describe Coeliac disease
- Coeliac sprue or gluten sensitive enteropathy
- Immune mediated enteropathy
Describe the pathogenesis of Coeliac disease
- Gliadin= Alcohol soluble component of gluten, contains most of disease-producing component, induces epithelial cells to express IL-15
- CD8+ Intraepithelial lymphocytes= IL-15–> activation/ proliferation of CD8+ IELs, cytotoxic & kill enterocytes, CD8+ IELs don’t recognise gladden directly.
What other diseases can Coeliac disease be associated with?
- Dermatitis herpetiformis
- Lymphocytic gastritis & colitis
- Enteropathy-associated T-cell lymphoma
- Small intestinal adenocarcinoma
