Pathology 3500 Lecture Notes - Lecture 4: Fibrinoid Necrosis, Growth Factor, Fat Necrosis
21 Mar 2018
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Lecture 4 - cell injury, adaptation and death iii. Irreversible cell injury: acute, severe stress or prolonged unrelieved stress, point of no return. Inability to reverse mitochondrial dysfunction (loose energy) too far cant fix machinery. Severe disruption of membrane function, point of too much disruption: eventually er gets separated from ribosomes - loose protein production, lysosomes empty into cell etc, all enzymes and parts in organelles gets released into cell. If the acutre stress is servere and exceeps the capaactiy of the cell to resepond , changes strucute and function lead to cell death. If the stress is prolonged and exceeds the capcacity of the cell to respond the cell will die. Necrosis intense esinophilia of cytoplasm (cell very pink or red: nuclear changes, pyknosis (shrinkage of nuc, karyorrhexis (breakup of nuclear material, karyolysis (dissolution of the nucleus) Inflammatory infiltrate - neutrophils (pnms) and macrophages ingest dead cells: only pathologic. In reversible injury nothing really happens to the nuc.
