Cellular Injury Flashcards
Type of cellular adaptation that ⬇️ in tissue mass due to ⬇️ in size and/or number of cells
Atrophy
Pathway that cell uses to ⬇️ size of tissue in atrophy
⬆️ cytoskeleton degradation via ubiquitin-protease pathway and autophagy.
Also ⬇️ protein synthesis
Earliest morphologic manifestation of reversible cell injury. Due to ⬇️ activity of Ca2+ and Na/K pumps
Cellular and mitochondrial swelling
Nuclear manifestations in irreversible cell injury
Pyknosis, karyorrhexis and karyolysis
DNA change indicative of cell apoptosis
Fragments in multiples of 180bp (DNA laddering)
Family of proteins that regulates apoptotic intrinsic (mitochondrial) pathway
Bcl-2 family.
BAX and BAK are proapoptotic, Bcl-2 and Bcl-xL are antiapoptotic
This apoptotic pathway needs Fas-FasL interaction, TNFα or cytotoxic T-cell release of perforin & granzyme B
Death receptor pathway (extrinsic)
Local inflammatory reaction due exogenous injury that leads to plasma membrane damage
Necrosis
Type of necrosis seen in ischemia/infarct, the injury denatures enzymes, preserved cellular architecture, eosinophilia
Coagulative necrosis
Type of necrosis seen in bacterial abscesses and brain infarcts, where neutrophils release lysosomal enzymes. Early → cellular debris and macrophages
Late → cystic spaces and cavitation
Liquefactive necrosis
Fragmented cells and debris surrounded by lymphocytes and macrophages
Granuloma
Mention the 2 subtypes of fat necrosis
- Enzymatic: acute pancreatitis
- Nonenzymatic: traumatic, like injury of breast tissue
This type of necrosis is due to immune complex deposition and/or plasma protein leakage from damaged vessel. Seen in PAN or preeclampsia
Fibrinoid necrosis
Gangrenous necrosis can be due two situations, which ones?
Dry gangrenous necrosis: ischemia
Wet gangrenous necrosis: superinfection
Neurons that are most vulnerable to hypoxic-ischemic insults
Purkinje cells of the cerebellum and pyramidal cells of the hyppocampus and neocortex