This is an English summary of pathology partial exam 2, given in second year biomedical sciences at vrije universiteit Amsterdam. My combined grade was 8 (1st exam 8.3, 2nd exam 7.7). The summary is based on lecture notes made in 2023.
Lecture 6 pathology of the gastrointestinal tract
Chapter 15 pages 590-636
Esophagus
Straight line between esophagus and stomach because of different endothelial lining Z-line. The
esophagus is lined with squamous epithelium, below this are fibroblasts and lymphocytes in lamina
propria and the muscularis mucosa. After this submucosa, lamina muscularis and adventitia.
Carcinoma
Esophageal carcinoma has two different pathways. The first pathway starts with long term reflux
esophagitis, having inflammation, hyperemia and in severe cases ulceration. This leads to intestinal
metaplasia, the squamous cells replaced by intestinal cylindrical epithelium for protection. Seen on
endoscopy by different color and Z-line. After this dysplasia occurs with molecular changes showing
in morphology as soon as the cells starts infiltrating in the wall this turns into an adenocarcinoma
(=Barrett carcinoma). The other type starts with a dysplasia of the squamous epithelium, evolving
into a squamous cell carcinoma.
Stomach
Gastric mucosa has same layers as esophagus, but different epithelial lining with foveolar layer and
glandular layer. 2 important types of glandular layer in corpus of stomach:
Parietal cells produce acid and intrinsic factor which binds to B12, in upper part
Chief cells produce pepsinogen, in deeper part
The antrum = lower part stomach with same foveolar lining but different glandular layer with
mucous producing cells and no parietal / chief cells. Also hormone producing cells and gastrin.
Inflammation and adenocarcinoma
There are two different types of gastritis caused by inflammation. The first is acute gastritis by
helicobacter pylori = one of only bacteria which can survive in stomach. Auto-immune gastritis
antibodies against parietal cells and / or intrinsic factor. Can lead to intestinal metaplasia and neuro-
endocrine cell hyperplasia (continuous gastrin secretion), anemia (no take up B12) and increased risk
for adenocarcinoma.
Gastric adenocarcinoma = intestinal type from intestinal metaplasia, still forms glandular
structures but very irregular. Diffuse type stomach wall thickened becomes tube like very stiff,
tumor cells are hard to detect because they are everywhere and do not form glandular structures
and can invade single cells. Prognosis is worse but treatment still the same. Neuroendocrine
(carcinoid) tumor = arise from neuroendocrine organs (Pancreas) and epithelia (G-cells).
Colorectal cancer
Small intestine can have obstructions through herniations (inguinal / femoral), adhesions,
intussusception (telescoping) and volvulus. Celiac disease = triggered by gluten, deaminated and
interact with T-cells for different HLA. Inflammatory bowel disease = inappropriate mucosal immune
activation by interactions with microbiota. Crohn’s disease = in terminal ileum and cecum, periods of
disease activity starts with ulcers and fissures.
Secondary prevention = detecting and screening before symptoms, focused on high risk groups
between 55-75. The program allows sampling at home which is then tested for blood in stool. In
colorectal cancer there is usually formation of polyps. Adenoma is dysplasia in the form of a polyp.
, Tubular adenoma = 2/3 of all polyps as dysplasia, the majority does not progress to CRC and this can
take many years. An advanced adenoma has high grade dysplasia, is bigger than 10 mm and has a
villous component. Adenoma turns into malignant polyp and carcinoma by molecular changes and
random mutations. Looking at size, the larger polyps are seen to be more malignant than smaller
ones. Same can be seen in histological classification and grade of dysplasia. However the smaller
ones occur more often and therefore all of them need to be removed. Cecal and right-sided colon
cancer is associated with iron-deficiency anemia, causing weakness and fatigue. Left-sided
adenocarcinomas may give bleeding and change in bowel habits.
Genomic instability is seen in 85% of all colorectal cancers. The other 15% by microsatellite
instability, point mutations etc. looking for the chromosomal abnormalities in the stool was not
effective. Structural abnormalities as point mutations would be easier to detect. Levels of molecular
changes can be at DNA, mRNA, miRNA and protein level.
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