Cell Death Flashcards
Causes of cell injury
Genetic defects Nutrition Lack of oxygen Physical agents (temperature, pressure, electricity, radiation) Chemicals and drugs Infectious agents Immune reactions
Reversible cell injury
As long as membrane stays intact then injury is most likely reversible e.g. fat accumulation and swelling due to loss of ion/fluid homeostasis
Apoptosis
Programmed cell death
Ordered, regulated process
Remains intact - using own energy to dismantle itself from inside out
Process of apoptosis
Normal cell -> condensation of chromatin -> membrane blebs-> cellular fragmentation forming apoptotic bodies -> phagocytosis of apoptotic cells and fragments removed without damage
Intrinsic mechanism of apoptosis
Balance of protein BCL-2 is disrupted, pro apoptotic proteins become dominant
Leading to the release of cytochrome C from the mitochondria which activates cascade 9 and then the final common pathway mediated by effector caspases
Extrinsic mechanism of apoptosis
Appropriate Ligand (E.g. FasL) bind with cell surface receptors that contain intracellular death domains e.g Fas
Activates effector route independent of mitochondrial factors —> activation of caspase 8 through death associated signalling complex which is regulated by proteins such as Fas-associated death domain protein
Activation of common executioner pathway
Intrinsic signals triggering apoptosis
Withdrawal of growth factors or hormones
Injury via radiation, toxins or free radicals causing DNA damage
Common executioner pathway
Triggered in both intrinsic and extrinsic mechanisms of apoptosis
Involves caspases 3,6,7
Activation of caspases
Via cleavage
Necrosis
Breakdown of plasma membrane, organelles and nucleus; leakage of cell contents
Liquefaction necrosis
Cell protein digested; loss of tissue architecture
Infiltration by inflammatory cells
Secondary infection by bacteria; wet gangrene
Occurs in lipid rich tissue
Coagulation necrosis
Only occurs when host stays alive
Cell proteins denature but are not disassembled resulting in ‘ghost outlines’
Cells lose nuclei and stain more deeply
If due to ischaemia then known as infarction
Caseous necrosis
End result of granulomas our inflammation
Granulomas are large areas of macrophages
Caused by autoimmune conditions and tuberculosis
Dry gangrene
Coagulation necrosis of extremity due to slowly developing vascular occlusion
Not a bacterial infection
Fat necrosis
Degradation of fatty tissue by lipases, forming chalky deposits
