College aantekeningen
Pathology DT1; volledige college aantekeningen 2022/2023
- Instelling
- Vrije Universiteit Amsterdam (VU)
Volledige college aantekeningen van het eerste deeltentamen van Pathology
[Meer zien]Voorbeeld 3 van de 24 pagina's
Voorbeeld 3 van de 24 pagina's
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Voorbeeld van de inhoud
Pathology DT1Hoorcollege 1: Introduction
Pathology
Pathology is the study of the cause and effects of disease or injury. The definition of
disease:
- Any abnormality that causes loss of health
- Characterized by a specific set of features that are not normal
Pathology is part of a disease’s systematic description: epidemiology, cause, pathogenesis,
clinical signs and symptoms, morphologic changes, complications and sequelae, prognosis,
mortality. Pathology provides information about all of this.
Prefixes: hyper, meta, hypo, etc. Suffixes: itis, oma, oid, etc. Eponym wanneer de ziekte
naar iemand is vernoemd.
Histology → biopsies, resections, frozen sections.
Cytology → fine needle aspirations, brushes, fluids, smears, urine, cerebrospinal fluid.
Course
All lectures will be recorded and put on canvas the same day. Exams are planned on site but
this can change to an at home exam pending a decision of the VU board of directors.
Lectures based on Robbins Basic Pathology (10th edition). You don’t have to read/learn the
whole book. Exact pages are indicated in the course schedules.
Exam 1 (45%) - 2-6.
Exam 2 (50%) - 10-13, 15, 19, 23.
CAT (5%) - workgroup assignment.
Learn the blue boxes (summaries) of the book and some examples of diseases. Quiz
questions are not typical exam questions.
Presentation of CAT by 2 persons of the group. Presentation of 8 minutes. 2 students will be
randomly selected. Discussion of 5 minutes. There also is a critical assessment task which
needs to be turned in on Canvas.
Digital practicals need to be completed before the exams!
Hoorcollege 2: Cell injury, Cell death and Adaptations (Ch2)
What is disease? Dysfunction of an organ tissue, because of damage to the cells. The
damage can be of many causes: chemical, thermal, radiation, DNA damage, microbacterial,
etc. The damaging agent is the etiology, the influence on and the changes in cellular
processes reflect the pathogenesis.
1
,In DNA: missense mutation (etiology radiation). CAT (triplet) codes for an amino acid, in this
case His. In a CAT sequence triplets can change due to a hit of a photon to CCT for
example, which changes the amino acid to Pro, this may cause a malfunctioning protein
(pathogenesis).
Radiation on DNA can cause a missense mutation which changes the amninoacid. That is
the pathogenesis, often of a sequence. Sikkel-cell is an example, this mutation changes
hemoglobin which causes malaria to be less attracted to them. However if you are exposed
to lower oxygen pressure the hemoglobin gets crystalized which causes them to get stuck in
blood vessels.
Etiology is an infection by bacteria, pathogenesis is the toxins created by a bacteria.
Rudolf Virchow was the first to realize that sickness can be traced back to a cell. Schleiden
and Schwann realized that there are different types of cells which can all cause different
diseases.
Cells are rarely alone, they are shaped and grouped together. They form a ‘community’, we
have billions of cells that make our bodies which are all very different.
The social amoeba Dictyostelium discoideum survives periods of food shortage by
organizing itself in a multicellular aggregate. Cooperation is very important. Multicellular
individuals; a niche in nature, with its own possibilities, but also its problems:
- Internal environment is optimized and thus also attractive for intruders. Effective
defense is required (infectious diseases)
- Organization & clear division of tasks is mandatory, incl. discipline of cells, a.o. with
regards to proliferation (cancer)
Cell damage & stressors:
- Disease is caused by damage to a cell or group of cells
- The initial damage can cause further damage
- The cell/organ reacts to minimize impact of damage
- Damage can be reversible, lead to adaptation or, ultimately death of the cell
2
, Myocardial infarction (right side of
picture) where the cells die because of
lack of oxygen (yellow patches). On the
left side the cells grew in size due to extra
stress load where they need to
compensate.
Hypertrophy → increase in the size of
cells, no increase in number of cells.
Myocardial hypertrophy can be caused
by mechanical stretch (increased workload, agonists and growth factors. It’s typically
seen in organs that show little mitotic activity.
Hyperplasia → increase in the number of cells, no increase in the size of cells.
Atrophy → decrease of tissue by decrease of cell size and/or number. Atrophy can be
caused due to cell loss (apoptosis),
Metaplasia → replacement of one tissue by another tissue.
There are different types of atrophy: autophagy, apoptosis, proteasomal degradation.
Different types of metaplasia: squamous metaplasia of bronchial epithelium (smoking),
Barrett's metaplasia (esophagus).
Cell damage by oxygen shortage: the cell swells. Cause: failure of NA/K-ATPase pump.
Happens a lot in the liver cells because they are very oxygen sensitive. The pumps won’t
work any longer which ultimately kills
the cell due to the water/salts balance
being disrupted.
There is necrosis and apoptosis.
Necrosis: pro-inflammatory, indices
repair and defense, cell contents are
released extracellularly, cellular
catastrophy (no regulation),
pathologic, occurs now and then.
Apoptosis: anti-inflammatory, no
induction of repair or specific defense,
cell contents are not released in
surroundings, cellular suicide under
strict regulation, part of normal
physiology, occurs continuously.
The main differences between necrosis and apoptosis are: the effect on inflammation, the
number of involved cells, the role in physiology and the initiation from within the cell.
3
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