Cell death Flashcards
types of cell death
oncosis
necrosis
apoptosis
oncosis
cell death with swelling, the spectrum of changes that occur in injured cells prior to death
necrosis
in a living organism, the morphological changes that occur after a cell has been dead for some time e.g. 12-24h
apoptosis
Cell death with shrinkage, induced by a regulated intracellular program where a cell activates enzymes that degrade it’s own nuclear DNA and proteins
types of necrosis
coagulative (main)
liquefactive (main)
caseous
fat necrosis
coagulative necrosis occurs in
ischaemia in solid organs
liquefactive necrosis occurs in
ischaemia in loose tissue
*presence of many neutrophils*
coagualtive necorsis due to
protein denaturation dominates over release of active proteases
liquefactive necrosis due to
enzyme release dominated over protein denaturation
what do cells that have undergone coagulative necrosis look like
cellular architecture is somewhat preserved-ghost outline
liquefactive necrosis lead to
liquefaction of tissue
- cell architecture lost
caseous necrosis is a distinctive form of
coagulative necrosis
- amphorous (structureless debris)
- tissue maintains a cheese-like appearance.
where does caseous necrosis occur
mainly in the lungs
- particularly associated with infection e.g. TB
fat necrosis
- Destruction in the adipose tissue
- Present in people with pancreatitis and in breast tissue after trauma
infarction
necrosis caused by reduction in arterial blood flow
• Can result in gangrene
gangrene
necrosis visible to the naked eye
• An appearance of necrosis
dry gangrene
necrosis modified by exposure to air (coagulative)
wet gangrene
necrosis modified by infection (liquefactive)
gas gangrene
Wet gangrene where the infection is with anaerobic bacteria that produce gas
what is an infarct
an area of necrotic tissue which is the result of loss of arterial blood supply
• An area ischaemic necrosis
apoptosis is
Cell death with shrinkage, induced by a regulated intracellular program where a cell activates enzymes that degrade it’s own nuclear DNA and proteins
Characteristic microscopic appearance
what does apoptosis look like
- Characteristic microscopic appearance
- Characteristic DNA breakdown
- Non-random, internucleosomal cleavage of DNA (in oncosis, DNA is chopped into pieces of random length)
apoptosis is the …. and …. force to mitosis
equal and opposite
characteristics of apoptosis
- Active process
- Single cell process
- Enzymes activated that degrade nuclear DNA and protein
- Membrane integrity is maintained
- lysosomal enzymes not involved
- Quick
- Pathological or physiological
1) Physiological apoptosis
- In order to maintain a steady state
- Hormone-controlled involution
- Embryogenesis
e. g. sculpting a hand during development
2) pathological apoptosis
- Cytotoxic T cell killing of virus-infected or neoplastic cells
- When cells are damaged, particularly with damaged DNA
- Graft versus host disease
How does apoptosis occur?
- Initiation
- Triggered by either intrinsic or extrinsic pathways
- Results in activation of caspases (enzymes which control and mediate apoptosis. Cause cleave of DNA and proteins of the cytoskeleton)
- Triggered by either intrinsic or extrinsic pathways
- Execution
- Degradation and phagocytosis
- Both pathways cause the cells to shrink and break into apoptotic bodies, which express proteins on their surface
- Now recognised by phagocytes or neighbouring cells
- Finally degradation takes place within the phagocytes/neighbour
intrinsic pathway
- Initial signal comes from within the cell
- Triggers:
- Irreparable DNA damage
- Withdrawal of growth factors or hormones
- P53 protein is activated and this results in the outer mitochondrial membrane becoming leaky
- Cytochrome C is released from mitochondria and activates caspases
Extrinsic
- Initiated by extracellular signals
- Triggers:
- Cells that are a danger e.g. tumour cells, virus-infected
- One of the signals is TNFalpha
- Secreted by T-killer cells
- Binds to cell membrane receptor (death receptor)
- Results in activation of caspases
- Triggers:
Apoptosis versus oncosis/necrosis
Ends of chromosomes are called telomeres, with every replication the telomere
is shortened.
When the telomeres reach a critical length, the cell can no longer divide
germ cells, stem cells and many cancer cells can produce
telemerase increasing the cells ability to replicates
Cell immortality
- As cells age they accumulate damage to cellular constituents and DNA
- After a certain number of divisions they reach replicative senescence - related to the length of chromosomes (telomeres)
