Cell Adaptation and Response to Stress Flashcards
cell injury can be –?
reversible - goes back to normal cell
irreversible - ends up in apoptosis or necrosis
hypertrophy
increase in size of cells. can increase organ size.
physiological: muscle in workout, uterus in pregnancy
pathological: heart wall thickness increases
hyperplasia
increase in cell number
physiological: hormonal trigger - breast tissue growth
compensatory - residual tissue growth after removal/loss ie. liver regrows after surgery to resect part.
pathological = excessive hormone = endometrial hyperplasia.
stimulus abated then hyperplasia disappears.
atrophy
decrease in cell size
causes = decrease work load, loss of innervation, aging, inadequate nutrition, diminished blood supply.
physiological & pathophysiological = same cell changes
aplasia & hypoplasia
aplasia = no cell proliferation hypoplasia = less cell proliferation
metaplasia
one cell type replaced by a different cell type that handles stress a little better.
can be malignant transformation
causes of cell injury
vascular: hypoxia (low O2) ischemia (no blood supply)
environment, infection, inflammation, inherited disorder, nutrional imbalance
general principles of cell injury
- depends on type of injury, duration and severity
- consequences depend on type, status, adaptability of injured cell
- injury results from functional and biochemical abnormalities.
Mitochondrial damage
decrease ATP (pumps relying on ATPfail, anabolic respiration = decrease pH, decrease protein synthesis)
increase ROS : damage caused by rate of production and removal. production>removal = membrane damage, protein misfolding, DNA damage.
entry of Ca2+
increase mt permeability = decrease ATPase to pump out ca2+ = decrease ATP. activate cellular enzymes = cell damage
plasma membrane
loss of cellular components - less ATP, osmotic imbalance
lysosomal membrane
leak enzymes - self-digestion
mechanisms to protect DNA from damage
- DNA repair enzymes
- apoptosis
- immune surveillance
necrosis
pathological process of cell death characterized by structured failure & injury to neighbouring cells *immune system activated
Never physiological
apoptosis
programmed cell death characterized by organized dissassembly and safe-guarding neighbouring cells.
physiologial - removve webbing btw fingers & toes in utero
pathological - radiation = apoptosis of skin cells.
morphology of necrosis
cytoplasmic changes & nuclear changes
cytoplasmic - enlarged cells , increase eosinophilia
nuclear - pyknosis (nuclear shrinkage & increase basophilia); karyorrhexis = fragmentation of shrunken nucleus; karyolysis = dissolution of chromatin.
patterns of necrosis
coagulative; liquefactive; caseous; fat necrosis; fibrinoid necrosis; gangrenous necrosis
coagulative necrosis
preserve outline of tissue
liquefactive necrosis
loss of tissue structure & surrounded by inflammation
bacterial/fungal, usually in brain.
caseous necrosis
collection of fragmented/lysed cells with amorphous granular pink appearance. tissue structure lost
fat necrosis
destruction due to release of activated lipase.
fibrinoid necrosis
deposition of immune complexes & fibrin produces pink amorphous fibrinoid.
gangrenous necrosis
no pattern
