Samenvatting
Samenvatting voor het tweede deeltentamen van Pathology
- Instelling
- Vrije Universiteit Amsterdam (VU)
Samenvatting van het tweede deeltentamen van Pathology.
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Voorbeeld 3 van de 22 pagina's
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Voorbeeld van de inhoud
Samenvatting Pathologie Deeltentamen 2Ch15: The Gastrointestinal Tract Hoorcollege
ESOPHAGUS
Normal situation:
Pinkish color is the wall of the esophagus and the darker area is the first part of the stomach.
The line is because there is a different epithelial lining in the esophagus and the stomach.
Microscope:
Squamous epithelium
A little bit of fibroblast and small amount of lymphocyte (lamina propria)
Muscularus mucosa on the lower part
These three layers form the mucosa
Fatty tissue and again some fibroblast and vascular
These are called the submucosa
Smooth muscle fibers and fatty tissue
Development of esophageal carcinoma:
Starts with esophagitis intestinal metaplasia dysplasia adenocarcinoma
Development of Squamous cell carcinoma
Dysplasia squamous cell carcinoma
Important to realize that these precursors (intestinal metaplasia) come before the tumor exist. If you
know that the lining of the esophagus is formed by squamous epithelial cells. If you develop a tumor
in that are it turns into squamous cell carcinoma. But also adenocarcinoma’s occur in the esophagus,
probably 2/3 of the tumors. Because of intestinal metaplasia (precursor lesion) it is possible for
adenocarcinoma to occur in places that are lined by squamous cells. Where the squamous epithelium
is replaced by cylindrical epithelium
The first step is long term esophagitis and in most cases that is reflux oesophagitis. That occurs when
the content of the stomach (which is very acidic) goes up in the esophagus and of course the
squamous epithelium is not made for the acid. You see al these little dots in between the epithelial
cells, those are neutrophils (inflammatory cells). When this keeps on existing and nothing is done, on
the long term it can lead to Intestinal metaplasia
Metaplasia is an important term to know. One type of cells is replaced by another type of cells that is
normally not present in this area. Glandular structures are formed and these normally do not occur in
the esophagus. Because of the constant irritation a differentiation starts going in another direction
and the cylindrical epithelial cells start to occur. Basically these cells are normal, they don’t have any
mutations, but just occurring at the wrong location. We call this intestinal type metaplasia, because it
basically looks like intestinal epithelium that we normally see in the bowel. The reflux still goes up in
the esophagus and on the long term molecular changes can start occurring. When that happens
dysplasia can occur.
On the long term when the inflammation keeps on continuing, than a molecular change can occur
and we see that through the microscope by changes in the morphology. Molecular changes go along
,with morphological changes. You don’t see the basal lining of the nuclei anymore and the amount of
cytoplasm has been reduced. Dysplasia severely increases the risk of developing adenocarcinoma.
Adenocarcinoma of the esophagus (Barret carcinoma). You can recognize large tumor masses. In the
microscope you can see glandular structures which infiltrate in the large muscular wall (muscularis
propria).
*The main difference between dysplasia and adenocarcinoma is that when you have dysplasia the
cells have molecular changes and they have mutations or chromosomal abnormalities, but the cells
are still located in the area where they are supposed to be. As soon as these cells start to infiltrate
and invading in the wall of the esophagus, than we call it an adenocarcinoma.
Dysplasia of squamous epithelium. Precursor lesion dysplasia which is similar to the precursor of
adenocarcinoma, but then we call it dysplasia of squamous epithelium. These cells are not invading
the lamina propria or deeper area’s of the esophagus.
Squamous cell carcinoma. These area’s of tumor cells infiltrate in the deeper walls of the esophagus.
Because it is derived from squamous epithelium, we call it squamous cell carcinoma. It has big
irregular cells.
STOMACH
Normal situation:
Gastric mucosa
Foveolar layer (make mucus)
Glandular layer
Two most important types of cells in the glandular layer
1. The parietal Cells
that are a bit pinkish
they produce acids and intrinsic factor (a very important protein, it binds to vitamin B12).
If you don’t have intrinsic factor, you mis the uptake of B12, which results in anemia.
2. Chief Cells
that are more blueish
they make pepsinogen. It is a protein that is important for the digestion of the food.
When it comes in contact with the acid stomach fluid, it breaks up in smaller molecules
pepsin.
*these two cells are just in the corpus, NOT present in the antrum of the stomach. The glandular
layer is more pale here than in the corpus. There are some hormone producing cells as well (eg.
Gastrin, which stimulates the production of acidic fluid by the parietal cells of the corpus part)
Smooth muscle (muscularis mucosae)
Inflammation of gastric mucosa (Gastritis)
Acute gastritis
H. pylori (helicobacter pylori) – bacteria that can cause inflammation in the stomach. Cells
are basically normal, but you can see curly lines at the surface of the cells and those are H.
pylori. Basically the only type that can survive in the acidic environment of the stomach.
Alcohol
NSAID
Auto-immune gastritis
, Antibodies are directed against parietal cells and intrinsic factor, these antibodies are made
by the body itself.
Intestinal metaplasia, similar to reflux
Neuro-endocrine cell hyperplasia, if you lose parietal cells you also lose this function. There
are G-cells in the entering part of the stomach. These regulate the acidity of the stomach
content. These gastrin producing hormonal cells, don’t know you have no parietal cells. The
PH of the stomach goes up, so they start produce more gastrin. This has no effect, because
the parietal cells are no longer there. It is hyperplasia of the G-cells in the antrum.
Anemia, because you lose intrincic factor (no intake of vitamin B12)
Increased risk for adenocarcinoma, that is the same mechanism as esophagus. When you
have intestinal metaplasia and you digest all types of food and bacteria which are not solved.
Bacteria can survive now and at some point molecular changes can occur.
*development of gastric adenocarcinoma: Normal mucosa chronic gastritis intestinal
metaplasia Dysplasia gastric adenocarcinoma
Increased risk for neuro-endocrine tumor
Others
…
Granulomatous gastritis, Crohn disease
2 types of adenocarcinoma in the stomach:
Intestinal type
It suggests that it is intestinal tumor, but it is not a bowel carcinoma. The term was used,
because the precursor lesion is intestinal metaplasia. Definition- it still forms glandular
structures. They are very irregular glands and it is important to release that glands are still
being formed.
Diffuse type
You don’t see a tumor area, that is because the tumor is everywhere. The wall is thickened of
the whole stomach. The wall is not expandable anymore. In some cases we can’t diagnose,
because it is difficult to see the tumor cells. These do not form glandular structures anymore
(they don’t stick to each other), they can invade a singular cell. They lost their adhesion
molecules. Worst prognosis in comparison to intestinal type.
Colorectal cancer development
*In the book pieces about inflammatory disorders of the colon, which are also very important.
GI tumors comprise 27% of alle cancer related mortality and it is present in late stage of the disease,
so then there is poor prognosis.
Different ways of cancer prevention
Primary prevention etiology
Secondary prevention pathogenesis
Colonrectal cancer screening program. You try to prevent the cancer to occur, but you also
try to treat it in a very early stage where it is still treatable with hopefully good prognosis.
Diagnostics pathogenesis
Therapy tumor biology
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