3. Irreversible Injury (cell death) Reversible Injury adaptation normal When cells encounter physiological stresses or pathological stimuli, they undergo adaptation, achieving a new a steady state and preserving viability. If the adaptive capacity is exceeded, cell injury develops. Within certain limits, injury is reversible. with severe and persistent stress, irreversible injury results.
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6. Incomplete occlusion of coronary artery Complete or prolonged occlusion hypertesion Prolonged starvation
101. Chemical nature of amyloid fibrils Two major forms: AL (amyloid light chain protein) AA (amyloid-associated protein): Derived from serum AA (12kd) synthesized in liver and elevated in inflammatory states.
102. Minor forms of amyloid fibrils: Transthyretin (TTR): A mutant form of a serum protein in familial amyloid polyneuropathy. A variant of TTR in aging. Beta-2-microglobulin (the component of class I MHC molecules) in long-term hemidialysis.
103. Minor forms of amyloid fibrils: Beta-2-amyloid protein forms the core of cerebral plaques and deposits within cerebral vessel walls in Alzheimer disease, deriving from a transmembrane glycoprotein precursor.
104. Minor forms of amyloid fibrils: Transthyretin (TTR): A mutant form of a serum protein in familial amyloid polyneuropathy. A variant of TTR in aging. Beta-2-microglobulin (the component of class I MHC molecules) in long-term hemidialysis.
105. Minor forms of amyloid fibrils: Beta-2-amyloid protein forms the core of cerebral plaques and deposits within cerebral vessel walls in Alzheimer disease, deriving from a transmembrane glycoprotein precursor.
171. Necrosis Apoptosis Stimuli Hypoxia Physical Toxins Pathological Histology Cell swelling Single cell Coagulation N Chromatin Disruption of condensation organelles Apoptotic bodies DNA Random Internucleosomal breakdown Diffuse
172. Necrosis Apoptosis Mechanism ATP depletion Gene activation Membrane Endonuclease injury Free radicals Tissue Inflammation No inflammation reaction Phagocytosis of apoptotic bodies
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175. Biochemical features of apoptosis 1.PROTEIN CLEAVAGE: Caspases (cysteine protease) Nuclear scaffold Cytoskeletal protein 2.PROTEIN CROSS-LINKING: Transglutaminase Cytoplasmic protein shrunken shalls apoptotic bodies Biochemical features of apoptosis
176. 3. DNA breakdown: 50-300 kb pieces Ca2+, Mg2+ dependent endonucleases DNA oligonucleosomes DNA ladders (also seen in necrosis) 4. PHAGOCYTIC RECOGNITION Receptors on macrophages for the surface components (phosphatidylserine, thrombospondin) on apoptotic bodies.
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183. normalcell Cellular swelling, chromatin cluping Membrane damage Nuclear chromatin condensation and fragmentation Cytoplasmic budding and apoptosisi body Phagocytosisi of apoptosis body The sequential ultrastructual changes in necrosis and apoptosis