Samenvatting
SUMMARY FOR FIRST EXAM PATHOLOGY
- Vak
- Pathology
- Instelling
- Vrije Universiteit Amsterdam (VU)
This is a whole summary for pathology.
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Voorbeeld 4 van de 47 pagina's
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Voorbeeld van de inhoud
Whole summaryLecture 1 Cell and tissue adaptation, &
damage
What is disease?
- Since 1830: origin of disease in cell
- Dysfunctional cells cause disease because of damage to the cells.
o Disease: not necessarily bad but can cause complications
- 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
o Ethiology: cause of disease
o Pathogenesis: changes in cell dues to disease
Example radiation
- Etiology: radiation
- Causes missense mutation in amino acid sequence
- Which will cause replacement of a single nucleotide
- Pathogenesis: incorrect protein
Example cholera
- Etiology: cholera
- toxin of bacteria will infect gut cells and will drawn cells of water can lead to diarrhea
- Pathogenesis: diarrhea
Community
- Cells are rarely alone, often shaped together in communities
Multicellular individuals
- a niche in nature, with its own possibilities, but also its problems
- Internal milieu is optimised which makes sure that cells are protected but also attractive for
intruders which want to make use for that for their own use
o So effective defence is required
- Organisation & clear division of tasks is mandatory, discipline of cells, proliferation
- Not all cells can do everything
- proliferation:
o Brain cells: can not divide because the pressure on the brain will be too large
o Liver: damage/take out part: new liver is formed, cells will divide rapidly
Example Dictyostelium discoideum
- multicellular by choice
- Communities might rise in need
, - The social amoebe Dictyostelium discoideum survives periods of food shortage by organising
itself in a multicellular aggregate.
Cell damage, stress & stressors
- Disease is caused by damage to (part of) a cell or group of cells (etiology)
- The initial damage can cause further damage (pathogenesis)
- The cell/organ reacts to minimize impact of damage (adaptation), or sometimes repair it:
way of dealing with damage by editing the cells
- Damage can be reversible, lead to adaptation or, ultimately to death of the cell
Adaptation (A) versus cell death (B)
Hypertrophy
- Hypertrophy: Increase in the size of cells, NO increase in number of cells
- Smooth muscles cells can’t divide: will become bigger
Example pregnancy
- even after still larger uterus
example high blood pressure
- Heart cells will need to perform more work
o Heart will adapt by increasing cell size, heart will increase in size as well
o More oxygen needed
o Signal transduction pathways activation will make more proteins to get contraction
apparatus going: all protein involved in contraction need to be increased to increase
the workload
o Bigger cells with more proteins
Hyperplasia
- Hyperplasia: Increase in the number of cells (not in the size of the cells)
Example Pregnancy
- breast will become bigger, due to increase in number
of cells because of lactation, more breast tissue needed
Hypertropy and hyperplasia
- both more and larger cells, called both the conditions
Atrophy
, - Atrophy: decrease of tissue by decrease of cell size and/or number
- Become smaller, does not matter id size or number of cells decreases
- Brain: decrease proven by weighing, gyri pattern is smaller and spaces
are wider
o Important for death people: can become smaller but also be the
same as few year ago shrinking of gyri shows that the brain used
to be bigger and heavier
o Alzheimer: looses brain cells
- Autophagy: cell destroys part of itself without killing
itself, cell will shrink and tissue will get smaller
- Apoptosis: cell suicide
- Proteasomal degradation: garbage clean up, smaller cell
Metaplasia
- Metaplasia: adaption to stressor, not ideal for epithelium type
- Replacement of one tissue by another tissue, both normal
o More cell layer: more resistant against stressors
- e.g. airway of smokers: cell lining in normal airways in one cell layer thick and vulnerable to
hot smoke, tissue will remodulate and form multilayer epithelium, if smoking will continue:
squamous epithelium can become abnormal and form cancer
Cell damage by oxygen shortage
- Cause: failure of Na+-K+-ATPase
- Main reason for cells to die/damage:
o unable to replenish energy stores
o causes swelling of cells
o no pumping out of: water, potassium, pump will
only pump when enough energy and oxygen,
o cells will blow up
- O2 loss: beginning reversible: replenish oxygen cell will shrink again and recover
o If it lasts for too long its irreversible cell will die
- Different per cell how long last without oxygen
o Nerve cell: notoriously short time without oxygen 5 min
o Heart: little bit longer
o Other cells: will survive longer but eventually will still die
Cell damage necrosis apoptosis
Necrose Apoptose
Pro inflammatory Anti-inflammatory
cells disintegrate inside of cell not in contact with surroundings, phagocyted
Induces repair and defence No induction of repair or specific defence
Cell contents are released extracellularly Cell contents are not released in surroundings
Cellular catastrophy no regulation Cellular suicide under strict regulation
Pathologic, never physiological Part of normal physiology
Occurs now and then Occurs continuously
Triggered by outside factors Triggered by inside factors
Necrosis
, types
Coagulation necrosis
- Vessel is blocked, tissue behind that get no oxygen
- No nuclei: death cells
- Structure of tissue still visible: but cells death
Colliquative necrosis (liquefactive necrosis)
- tissue severely damaged, wait long enough, hole will be formed and whole
area will disappear, typical for the brain, not visible in many other organs
Caseous necrosis (TBC)
- caused by bacterial infection, called this because it looks like French
cheese, typical for tuberculosis
Fat necrosis (in pancreatitis)
- Necrosis in fatty tissue, caused by chemical compounds released from fatty
tissue, which are very irritative
Fibrinoïd necrosis (arterial wall)
- Vessel walls: looks like fibrin
Regulated elimination and replacement
Proteins Proteasomal degradation and new synthesis
Parts 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
Apoptosis
When apoptosis?
- Embryonal development (‘programmed cell death’): brain: made by huge amount of cells of
which majorly will die by apoptosis
- Normal tissue homeostasis (cell death and formation of new cells)
- Selection of early maturational stages of lymphocytes by antigen receptors
- Involution or atrophy (endometrium during periods; breasts after lactation, &c.)
- Termination of inflammatory response or immune reaction
- Elimination of virus-infected cells or cells with (oncogenic and other) mutations, by CTL
- Eliminaton of stressed cells by NK cell
- Elimination of damaged cells
overview of the mechanism
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