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L3 Cell Injury & Death


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cell injury
biochemical and/or morphological changes that occur when the steady state is perturbed by adverse influences (injurious stimuli or failure to adapt)
adaptation
consequence of stress
hyperplasia
increased cellular activity: more cells in response to stress
hypertrophy
increased cellular activity: bigger cells in response to stress
atrophy
decreased cellular activity due to decreased stress
metaplasia
transformation of one type of differentiated cell into another fully differentiated cell type (e.g. columnar epithelial to squamous epithelial due to smoking); occurs in the context of alterations in the cellular environment, especially in context of chronic cell injury and repair
mechanical injury
AETIOLOGY: trauma, osmotic pressure; MECHANISMS: rupture of cell membrane
energy failure
AETIOLOGY: thrombus blocks vessel (decreased O2 + glucose); MECHANISM: ATP depletion
ionising radiation
AETIOLOGY: UV rays, X-rays, radioactive particles; MECHANISM: generation of free radicals and direct damage to macromolecules (e.g. thymine dimer formation in DNA)
free radicals
very reactive moluecules that want to steal electrons from other molecules, altering chemical bonds in process
infectious organism
AETIOLOGY: _________ __________; MECHANISM: bacterial toxin - exotoxins & endotoxins; hijacking of cell machinery by viral infection (cell lysis); collateral damage by inflammation
exotoxins
a toxin released by a living bacterial cell into its surroundings
endotoxins
a toxin present inside a bacterial cell that is released when it disintegrates
chemical injury
AETIOLOGY: 'poisons'; MECHANISMS vary - e.g. lead, cyanide, arsenic, tobacco, alcohol
apoptosis
programmed cell death that doesn't damage adjacent cells; signals cause death; no harmful products; requires energy
Lead
blocks synthesis of haemoglobin
necrosis
abnormal, unintended cell death that causes damage to surrounding tissue; response to cell injury; release of harmful products; does not expend energy
Cyanide
blocks electron transport chain (complex III)
physiological
p________ signals for apoptosis: embryogenesis, involution, elimination of self-reacting lymphocytes
pathological
p________ signals for apoptosis: DNA/protein damage, viral infections, cell killing by cytotoxic T-cells, chemo/radiotherapy
FAS receptor
Extrinsic Death Signal (apoptosis)
DNA damage
Intrinsic Death Signal (apoptosis)
inhibit
growth factors and cell attachment _______ apoptosis
Bcl-2
family of anti-apoptotic proteins on mitochondrion that interpret signals
Caspase
molecules that cause apoptotic bodies to form
Follicular Lymphoma
Carcinogenic apoptosis dysfunction: anti apoptotic BCL-2 over expressed: inhibits apoptotic cell death & cells accumulate
coagulative
form of necrosis: most common type; denaturation of intracytoplasmic protein; dead tissue firm and slightly swollen; retention of microscopic architecture in dead tissue; typical of ischaemic injury (except brain)
colliquative
form of necrosis: in brain; neural tissue has little supporting tissue and thus liquifies upon cell death; site eventually marked by a cyst
caseous
form of necrosis: characteristic of TB, 'cheese-like'; granulomatous inflammation; dead tissue lacks any structure
gangrenous
form of necrosis: either wet or dry; non-distinctive pathology (surgical term)
dry gangrene
gradual hypoxic coagulative necrosis of lower limbs
wet gangrene
liquefactive action of superimposed bacterial infection on gangrene; prone in bowel infarct