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Lectures notes Pathology partial exam II

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  • Course
  • Pathology (AB_1202)
  • Institution
  • Vrije Universiteit Amsterdam (VU)
  • Book
  • Robbins Basic Pathology

This document contains extensive notes of the lectures that belong to partial exam II. For the first exam I had a 9,7! Many pictures are included with an explanation as clear as possible. It is in it English because the exam will also be in English. The practice questions of the lectures are also i...

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  • March 19, 2022
  • 83
  • 2021/2022
  • Class notes
  • Dr. jeroen hoozemans, dr. marianna bugiani
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Lectures Pathology deeltentamen II




Index
Lecture 1 – Chapter 15: Pathology of the digestive tract........................................................................ 2
Lecture 2 – Chapter 15: The lung .......................................................................................................... 12
Lecture 3 – Chapter 12: The hematopoietic and lymphoid systems Part I .......................................... 24
Lecture 4 – Chapter 12: The hematopoietic and lymphoid systems Part II .......................................... 32
Lecture 5 – Chapter 10: Atherosclerosis and Chapter 11: The heart .................................................... 39
Lecture 6 – Chapter 19: The Female genital system ............................................................................. 53
Lecture 7 – Chapter 23: Neuropathology .............................................................................................. 64
Lecture 8 – Chapter 23: Prion disease and neurodegenerative diseases ............................................. 75




1

,Lecture 1 – Chapter 15: Pathology of the digestive tract
PART I – UPPER DIGESTIVE TRACT

Normal esophagus
- The junction between esophagus and stomach epithelium → Z-line.
- Different layers:
o Mucosa:
▪ Luminal part → Squamous epithelium.
• Squamous cells stacked on top of each other.
• At the bottom of the epithelium (just above the lamina propria)
proliferation of the squamous epithelium occurs.
• The cells differentiate and migrate towards the lumen side (surface)
of the epithelium.
▪ Lamina propria.
▪ Muscularis mucosa.
o Submucosa:
▪ Fatty tissue.
▪ Fibroblasts.
▪ Blood vessels.
▪ Nerves.
o Circular muscular layer.
o Longitudinal muscular layer.
o Adventitia → Outside layer.
▪ Mainly fatty tissue.
▪ Layer that neighbors the other organs.

Development of esophageal carcinoma:
- 2 types of carcinoma:
o Esophagitis → Intestinal metaplasia → Dysplasia → Adenocarcinoma.
▪ Esophagitis → Reflux of fluids from the stomach, can start inflammation.
▪ Intestinal metaplasia → Cells differentiate in another direction because of
the inflammation in order to protect the esophagus from the acid.
• We call it intestinal because the cells start to differentiate into cells
that look similar to the epithelial cells of the stomach → Cylindrical
cells.
o Dysplasia → Squamous cell carcinoma.
- Very different kinds and they have different behaviors.
o Treated in different ways because they have different molecular backgrounds.
- You would expect that the cancer cells deprive from the cells the epithelium is made of thus
→ Squamous epithelium.
o However, this type of cancer is very rare.
- Instead the squamous epithelium start to change to
intestinal epithelium and this epithelium can give rise to a
tumor leading to → Adenocarcinoma.
o Most prevalent one.



2

,Reflux esophagitis
- Phase 1 → Inflammation.
o Hyperemia → Increased blood flow.
o Granulocytes → Neutrophils.
▪ Leads to a very crowded lamina propria.
o In severe cases ulceration.
- Phase 2 → Metaplasia and (chronic) inflammation.
o When the reflux and thus the inflammation becomes chronic.
o Metaplasia → Replacement of a differentiated cell type by another
differentiated cell type.
o The new cells look like bowel cylindrical epithelium.
▪ These cells form glands that produce mucus.
▪ These cells are not neoplastic → Don’t have
any molecular changes in the genome.
o Metaplasia → Normal cells but in the wrong place.

Intestinal metaplasia
- Squamous epithelium is replaced by intestinal
type epithelium.
- Barret esophagus = Intestinal metaplasia.
o Close to the junction between esophagus
and stomach the esophagus wall is red →
Indication of intestinal metaplasia.

Dysplasia of intestinal metaplasia
- Dysplasia → Abnormal growth.
o Now it becomes dangerous → Risk to develop cancer.
- Cytonuclear atypia → Abnormal nucleus.
o Large nuclei.
o Irregular shape of nuclei.
o Coarse chromatin pattern.
- When the dysplasia progresses, you won’t recognize the goblets cells anymore
because of mutations.
- Dysplasia is still not an invasive cancer but the cells do have abnormal DNA because of
mutations.
o The cells are still located on the right space where they should be.

Adenocarcinoma of the esophagus → Barrett carcinoma.
- The cells are now invasive and they migrate into the deeper layers of the esophagus.




3

, Dysplasia of squamous epithelium
- Usually located a little bit higher in the esophagus than
adenocarcinoma.
- Same characteristics as dysplasia of intestinal metaplasia:
o Abnormal shape of the nucleus.
o Large nucleus.
o Coarse chromatin pattern.
- Dysplasia is only in the squamous epithelium and no other layers.

Squamous cell carcinoma
- The abnormal cells start to invade the other layers of the esophagus.
- Deeper invasion → Poor prognosis.

Normal stomach
- Your stomach has folds so it can expand when you eat.
- Gastric mucosa → Histology.
o Stomach is lined with cylindrical epithelium.
o On top → Foveolar layer.
▪ Gastric pits.
▪ Mucus cells.
o Glandular layer
▪ Many different cells.
▪ Most important cells → Parietal cells →
Make acid and intrinsic factor.
o Smooth muscle layer.
- Lamina propria is not really an layer but is very little between the glandular cells to give
support.
- Histology of the antrum → Lower part of the stomach.
o Have the same layers as the rest of the
stomach.
o Difference → In the glandular layer there
are no parietal cells, instead it contains
hormone producing cells that produce
gastrin → Stimulates the parietal cells in the
corpus of the stomach to produce acid.

Inflammation of the gastric mucosa → Gastritis.
- Acute gastritis:
o H. pylori.
o Alcohol.
o NSAID → Anti-inflammatories.
- Auto-immune gastritis.
- Others:
o Granulomatous gastritis, Crohn’s disease.
o Lymphocytic gastritis.
o Others.




4

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