Cell Injury II Flashcards
two forms of cell death
necrosis or apoptosis
features of necrosis
swelling, accidendal, entire region affected. inflammation is key. biochemical changes occur early on. increased permeability. proteins denatured
coagulative necrosis
tissue agriculture preserved, common in ischemia, inflammation and logs of macrophages (the visible nuclei). cell swelling. Nuclear changes. nearby cells lighter due to hydrophobic change
caseus necrosis
cottage cheese. common in TB. calcified center, rings of macrophages/fibroblasts. multinucleated giant cells. Epitheloid cells.
liquefactive necrosis
infections (bacterial or fungal), hypoxic cells in CNS, complete digestion of dead material. “cyst” may remain (stroke)
fat necrosis
focal fat distraction, pancreatic damage releases lipase, which release triglycerides. These can interact with calcium. Saponification.
apoptosis
programmed cell death. Subtle, caused by irreversible damage. energy depended, coordinated process. Cells shrink, then bleb. regulation can be intrinsic or extrinsic.
example of apoptosis
follicular atresia
mitochondria issues can cause both
necrosis (radiation/toxin/low02) or apoptosis (DNA/protein damage)
intracellular accumulation causes
abnormal metabolism, protein formation issues, lysosomal storage diseases (lack of enzyme), exogenous material intake
calcium deposits can be
normal or path. Path: dystrophic, metastatic
dystrophic calcium
normal in body, only abnormal in nonviable or dying tissue. Abnormal deposition.
metastatic calcium
abnormal metabolism leads to increased serum levels. Caused by vitamin D issues, hyperparathyroidism, etc. hypercalcemia in normal tissues itself doesn’t cause dysfunction
morphology of necrosis
eosinophilia and nuclear changes
apoptotic signaling
extrinsic- death receptor, cascade cascade
intrinsic- mitochondria MPTP pathway
