Chapter 15: the gastrointestinal tract
Upper digestive tract:
Normal oesophagus got a z-line, part to the stomach. The oesophagus contains squamous
epithelium (E), lamina propria, (L) muscularis mucosa (MM) form the mucosa.
The squamous epithelium is stacked upon each other, with underneath stem cells.
2 types of carcinomas in the oesophagus:
1. Oesophagitis, reflux cause inflammation. Hyperemia, granulocytes and in severe cases
ulceration> intestinal metaplasia, so differentiate in other direction then should have. Can
be glandular cells producing mucus > dysplasia, resulting in large nuclei, irregular shape of
nuclei and coarse of chromatin pattern. But this is still not invasive. > adenocarcinoma
(Barrett), invading other tissues than the upper epithelial tissue.
2. Dysplasia, located higher in oesophagus. > squamous cell carcinoma, no clear division
between the layers
Stomach:
Layers: foveolar > glandular > smooth muscle.
In the corpus: In the gland, mucous cells are present for protection of the stomach. Also the parietal
cells are present which make the acid.
In the antrum: in the gland, no parietal cells. Do have mucous cells and hormone producing cells.
Inflammation of the gastric mucosa:
- H. pylori. Bacteria that can live in the acidic environment. Resulting in ulcers.
- Auto-immune gastritis. Antibodies against the parietal cells and intrinsic factor. Causing
intestinal metaplasia, endocrine hyperplasia, anaemia (uptake B12 is reduced because no
intrinsic factor made by the parietal cells). Increased risk for adenocarcinoma & neuro-
endocrine tumor.
Due to the chronic inflammation in both cases, first morphological changes, and later genomic
changes, which could result in gastric adenocarcinoma. No squamous cell carcinoma. 2 types,
intestinal and diffuse type (worse prognosis).
Lower digestive part:
GI tumours has high incidence rate. Secondary prevention is population-based screening, to early
detection and identify patients with high risks.
Normal epithelium can progress into 4 things:
1. Hyperplastic polyps
2. Adenoma > dysplasia > adenocarcinoma. 2/3 of all polyps. But the 95% of these adenomas
does not progress to carcinomas, because that take mostly 10-15 years. Advanced
carcinoma can be seen by high grade dysplasia, size & villous component
3. Inflammatory polyp
4. Peutz-jeghers polyp
Size: above >2 cm, 72% of malignancy. But the 1-2 cm is 20% of all cancers.
Villous: all types are in 1/3 of the category of the cancers. So cannot focus on one.
Dysplasia: all types are in 1/3 of the category of the cancers. So cannot focus on one.
So this cannot be used in the screening programme.
Accumulation of different mutation > wrong combination > could give a carcinoma.
Genomic instability:
1. Chromosomal instability. Number of copies is different and structural changes. 85% of
cancers in 8p-, 8q+, 13q+, 20q+, 15q-, 17p- and 18q-.
2. Microsatellite instability. MSS and MSI
Protein biomarkers is also used so search for advances adenomas and carcinomas.
Upper digestive tract:
Normal oesophagus got a z-line, part to the stomach. The oesophagus contains squamous
epithelium (E), lamina propria, (L) muscularis mucosa (MM) form the mucosa.
The squamous epithelium is stacked upon each other, with underneath stem cells.
2 types of carcinomas in the oesophagus:
1. Oesophagitis, reflux cause inflammation. Hyperemia, granulocytes and in severe cases
ulceration> intestinal metaplasia, so differentiate in other direction then should have. Can
be glandular cells producing mucus > dysplasia, resulting in large nuclei, irregular shape of
nuclei and coarse of chromatin pattern. But this is still not invasive. > adenocarcinoma
(Barrett), invading other tissues than the upper epithelial tissue.
2. Dysplasia, located higher in oesophagus. > squamous cell carcinoma, no clear division
between the layers
Stomach:
Layers: foveolar > glandular > smooth muscle.
In the corpus: In the gland, mucous cells are present for protection of the stomach. Also the parietal
cells are present which make the acid.
In the antrum: in the gland, no parietal cells. Do have mucous cells and hormone producing cells.
Inflammation of the gastric mucosa:
- H. pylori. Bacteria that can live in the acidic environment. Resulting in ulcers.
- Auto-immune gastritis. Antibodies against the parietal cells and intrinsic factor. Causing
intestinal metaplasia, endocrine hyperplasia, anaemia (uptake B12 is reduced because no
intrinsic factor made by the parietal cells). Increased risk for adenocarcinoma & neuro-
endocrine tumor.
Due to the chronic inflammation in both cases, first morphological changes, and later genomic
changes, which could result in gastric adenocarcinoma. No squamous cell carcinoma. 2 types,
intestinal and diffuse type (worse prognosis).
Lower digestive part:
GI tumours has high incidence rate. Secondary prevention is population-based screening, to early
detection and identify patients with high risks.
Normal epithelium can progress into 4 things:
1. Hyperplastic polyps
2. Adenoma > dysplasia > adenocarcinoma. 2/3 of all polyps. But the 95% of these adenomas
does not progress to carcinomas, because that take mostly 10-15 years. Advanced
carcinoma can be seen by high grade dysplasia, size & villous component
3. Inflammatory polyp
4. Peutz-jeghers polyp
Size: above >2 cm, 72% of malignancy. But the 1-2 cm is 20% of all cancers.
Villous: all types are in 1/3 of the category of the cancers. So cannot focus on one.
Dysplasia: all types are in 1/3 of the category of the cancers. So cannot focus on one.
So this cannot be used in the screening programme.
Accumulation of different mutation > wrong combination > could give a carcinoma.
Genomic instability:
1. Chromosomal instability. Number of copies is different and structural changes. 85% of
cancers in 8p-, 8q+, 13q+, 20q+, 15q-, 17p- and 18q-.
2. Microsatellite instability. MSS and MSI
Protein biomarkers is also used so search for advances adenomas and carcinomas.
