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Pathology lectures summary (midterm 1)
- Instelling
- Vrije Universiteit Amsterdam (VU)
Summary of all Pathology lectures (for midterm 1).
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PTL lecture CH2: Cell injury, cell death and adaptationsWhat is disease? (= dysfunction of an organ or tissue, because of damage to the cells)
> the damage can be of many causes
- chemical, thermal, radiation, DNA damage, microbial, etc.
> cause and consequence
- cause = etiology (the damaging agent)
- consequence = pathogenesis (the influence on and the changes in cellular processes reflect
the pathogenesis, e.g. change in DNA or amino acid sequence)
> community
- multicellular organisms: a niche in nature with its own possibilities, but also problems
- infectious diseases → internal milieu is optimised, and thus also attractive for intruders so
effective defence is required
- cancer → organisation and clear division of tasks is mandatory (including discipline of cells,
i.e. with regards to proliferation)
Cell damage, stress and stressors
> damage to cells can be reversible, lead to adaptation, or ultimately to the death of the cell
- adaptation = the cell/organ reacts to minimize the impact of the damage
- i.e. in the case of cancer, if the damage to the DNA is severe , it is better to induce cell
death to avoid cancer
> cell tissue and adaptation
- hypertrophy = increase in the size of the cells, no increase in the number of cells
- myocardial hypertrophy
- mechanical stretch (increased workload), agonists and growth factors induce signal
transduction pathway, which leads to the synthesis of transduction factors and
subsequently the regulation of gene transcription (of contractile proteins)
- hyperplasia = increase in the number of cells, not in the size of cells
- atrophy = decrease of tissue by decrease of cells size and/or number
- to adapt an organ/tissue so that they don’t take up nutrients that aren’t necessary
for them when they’re inactive
- proteasomal degradation: ubiquitin binds to the molecule that needs to be
degraded so that the proteosome can recognize and degrade it
- autophagy: in order to save resources, the cell takes up and degrades the
organelles that aren’t necessary
- apoptosis
- metaplasia = replacement of (normal tissue) by another (normal) tissue
- i.e. when normal columnar epithelium in the airways gets replaced by squamous
metaplasia (= an adaptation to when someone smokes cigarettes)
- pro: bronchia are protected from the hot smoke entering your lungs
- con: the cilia on top of the normal epithelium are now gone, so all the
mucus (containing bacteria and other pathogens) stays in your airways, because the
clearance is hindered
,> atrophy: necrosis and apoptosis
- necrosis
- = pathologic! (occurs every now and then)
- happens to a group of cells
- cell gets injured → if reversible, cell recovers. If irreversible, injury progresses,
leading to swelling (shows up as light staining in a preparation)
- organelles swell up, contents of the cell gets broken down and leaks
- eventually, the cell bursts and the immune system gets activated (inflammation),
which leads to further damage (PRO-inflammatory)
- apoptosis
- = part of normal physiology! (occurs continuously)
- (often) happens to individual cells
- cell gets irreversibly damaged → chromatin condenses and the cell starts to get
fragmented and becomes smaller (shows up as dark staining in a preparation)
- fragments of the apoptotic cell gets phagocytized by surrounding phagocytes, so
there is NO inflammatory response (ANTI-inflammatory)
- kidney cells: oxygen shortage causes cell damage (cell swells), since oxygen is needed to
replenish ATPase, which is needed for a functional Na/K-ATPase pump. When there is no
oxygen, K moves out of the cell and Na moves into the cell, [Na] goes up → cell takes up
water and swells
- types of necrosis
- coagulation necrosis: accidental cell death caused by ischemia (lack of blood
flow/O2) or infarction (indicated by the lack of nuclei)
- colliquative necrosis: the damaged tissue turns into a liquid viscous mass (typical
for the brain, also called liquefactive necrosis)
- caseous necrosis: in the case of tuberculosis
- fat necrosis: in case of pancreatitis, cells of the pancreas die and pancreatic
enzymes are no longer being made. The fatty acids in the fat cells take up calcium,
which appears as white spots on the pancreas
- fibrinoid necrosis: only appears in the arterial wall when blood vessels are
inflamed, the necrotic tissue resembles fibrin (hence the name)
, Regulated elimination and replacement
> = a central theme in biology
- proteins: proteasomal degradation and new synthesis
- part of cells: autophagy and new synthesis
- cells: apoptosis and compensatory cell division
- tissues: menstrual cycle, regrowth of liver after partial removal
- organism: death and reproduction
> when to undergo apoptosis?
- embryonal development: programmed cell death to from fingers
- normal tissue homeostasis: cell death and formation of new cells
- selection of early maturational stages of lymphocytes by antigen receptors
- involution (shrinkage of useless organs) or atrophy: endometrium during periods, breasts
after lactation
- termination of inflammatory responses or immune reactions (since strong inflammatory
responses can cause damage)
- elimination of virus-infected cells or oncogenic/mutated cells by cytotoxic T cells (CTL)
- elimination of stressed cells by NK cells
> apoptosis mechanisms
- extrinsic pathway
- ligand binds to and activates the death receptor
on the cell (a lethal signal from outside the cell
(FasL, tumor necrosis factor (TNF)) triggers a
cascade that leads to apoptosis)
- cell starts digesting itself with caspase enzymes,
which are activated by the receptor-ligand
interaction
- intrinsic pathway (mitochondrial), see picture
- lack of survival signals → anti-apoptotic
proteins, such as BLC2 and BCL-XL, are no longer
synthesized → cytochrome C starts leaking from
the mitochondria due to the activation of the
BAX/BAK channels → cytochrome C activates
caspases → apoptosis
> BCL2 and B cell (follicular) lymphoma
- follicular lymphoma is a cancer that
affects white blood cells (lymphocytes)
- loss of apoptosis response due to
overexpression of the BCL2-gene (caused
by translocation, BCL2-gene is brought
under control of the promotor of the
heavy chain of the immunoglobulin)
> apoptosome
- cytochrome C binds to Apaf-1 (apoptosis-activating factor-1), forming a heptamere
- this heptamere complex binds to procaspase-9 and ATP, activating procaspase-9 and the
cascade of caspase-activation ensues
- basically the apoptosome activates caspase-9
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