Flashcards in MOD 3 - Cell Injury Deck (44):
in cellular adaptation, increased cellular activity = ?
in cellular adaptation, decreased cellular activity = ?
in cellular adaptation, change in cell morphology = ?
what are the 9 common aetiology of cell injury
physical trauma, oxygen availability, chemical agents, infectious organisms, irradiation, others - immunological, lack of essential nutrient/vitamin, genetic disorders, ageing
what are the 2 main causes of physical trauma?
mechanical trauma - disruption of cells & thrombosis leading to ischaemia, extremes of temperature - heat denatruration of proteins, ice crystals, fever
what are the 2 main causes of oxygen availability ?
hypoxia/anoxia - reduction or loss of oxygen delivered to cells often caused by ischaemia, reoxygenation - reprefusion - can generate oxygen free radical which can lead to further cell death ie reprefusion injury
what are some of the common chemical agents which can cause cell injury
alcohol, tobacco smoke, drugs, poisons, environmental, occupational
what are the common mechanism which infectious organisms cause cell injury
bacterila toxi - exotoxins & endotoxins, hijacking of cell machinery by viral infection - cell lysis, collateral damage by inflammation.
what happen to the level of Ca2+ should mitochondria is damaged as part of cell injury
ATP drop - Na pump deactivate - Ca2+ influx along with H2O, Na - cell swell
what happen to the level of pH should mitochondria should fail
ATP drop - glycolysis increase (anaerobic production of ATP - lactic acid) - pH drops - nuclear chromatin clumping
what happens to the level of protein synthesis should mitochondria should fail
ATP drops - ribosomes detachment - decreased protein synthesis - lipid deposition within the cell (steatosis) (usually exported accompanied by exportation of protein) ie fatty change / cloudy swelling
what is a free radical?
it is a highly reactive ions/molecules with single unpaired electron in outer orbital eg oxygen free radicals
what does free radical do to proteins and nucleic acids & cel membrane?
chain reaction with the cell membrane to produce more free radical, damages proteins and nucleic acid - causing apoptosis
how is free radical detoxified
by superoxide dismutase and antioxidants eg vitamins A, C&E
what does superoxide do in our body?
bacterial killing by neutrophils and macrophages depends on superoxide (another reaction used by the body to produce free radical for its own good)
what happens when cell membrane is defective?
loss of membrane barriers leads to break down in metabolite gradients - increased Ca2+ which activates a number of enzymes eg ATPase (ATP depletion), prtoeases (break down membrane& cytoskeletal proteins), endonuclease (responsible for DNA fragmentation)
what is necrosis?
cll death as a result of lethal cell injury - passive process
what will necrosis incite?
what are the subtypes of necrosis?
coagulative (most common), caseous (only happen in TB), Colliquative (only happen in brain), gangree (wet and dry subtype), fat & fibrinoid
state a description of coagulative necrosis
denaturation of intracytoplasmic proteins which then turn the tissue firm and slightly swollen and in normal setting tissue will have retention of microscopic architecture but protein within the dead cells can leak into blood stream
what is common condition for coagulative necrosis?
ischaemic injury (except in brain)
what is colliquative necrosis
it is necrotic neural tissue which is subject to total liquefaction and the site is eventually marked by a cyst
what is caseous necrosis characteristic of?
what is caseous necrosis like?
cheese like - cellular detail destroyed then surrounded by granulomatous inflammation, no cellular structure can be identified
what is the difference between apoptosis and necrosis?
in apoptosis, cell membrane remain intact and no inflammation reaction and necrosis is the total opposite
what is gangrenous necrosis?
it is necrosis with putrefaction of the tissue (sometimes due to infection of certain bacteria such as clostridia) which will appear as black due to the deposition of iron sulphide from degraded haemoglobin
example of 'wet' gangrene?
complication of appenditis, intestinal necrosis - clostridia common in bowel
example of 'dry' gangrene
usually seen in toes etc as results of gradual arterial or small vessels obstruction in cases of diabetes or atherosclerosis
does apoptosis require energy to be carried out?
yes - active process
what is the enzyme which is responsible for carrying out apoptosis?
what are the 2 enzymes which activates caspases
AIF (apoptosis initiating factor) & cytochrome C
where are AIF & cytochrome C normally sequester?
what enzyme normally sequester caspases and what normally down-regulate it?
Bcl-2 which is normally sequester by p53.
what can cause extrinsic pathway to commence?
what can cause intrinsic pathway to commence?
radiation & damages to DNA
which one of the necrosis and apoptosis will affect multiple cells?
which one of the necrosis and apoptosis will cause reduced size cells?
what happens to the nucleus of the cells which underwent necrosis?
pyknosis - karyorrhexis - karyolysis
which one of the necrosis and apoptosis will have intact plasma membrane?
which one of the necrosis and apoptosis will have intact cellular contents?
which one of the necrosis and apoptosis will cause adjacent inflammation
what is pyknosis
process which cause cell nucleus to thicken into a dense mass which occurs when cells die
what is karyorrhexis
fragmentation of cell nucleus