I - Cell Injury, Cell Death and Adaptations Flashcards
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Increase in size of cells resulting in increased size of organ.
Hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3
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Increase in number of cells.
Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3
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Hypertrophy of hyperplasia?Uterus during pregnancy
Both Estrogen stimulated SM hyperthrophy and hyperplasia (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3
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Hypertrophy or hyperplasia?Wound healing
Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.4
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Type of cell death characterized by nuclear dissolution, without complete loss of membrane integrity.
Apoptosis(TOPNOTCHRobbins Basic Pathology, 8th ed. p.7
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Type of cell death which is energy-dependent, tightly regulated, and associated with normal cellular functions.
Apoptosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.7
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Type of cell death which results from a pathologic cell injury.
Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.9
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Type of cell death associated with inflammation.
Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
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It is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis.
Pyknosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
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It is the destructive fragmentation of the nucleus of a dying cell.
Karyorrhexis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
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It is the complete dissolution of the chromatin of a dying cell.
Karyolysis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
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This is the first manifestation of almost all forms of injury to cells.
Cellular swelling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.8
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Small clear vacuoles within the cytoplasm, representing pinched-off segments of the endoplasmic reticulum.
Hydropic change or Vacuolar degeneration (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23
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Appearance of lipid vacuoles in the cytoplasm.
Fatty Change(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23
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Surface blebs, increased eosinophilia of the cytoplasm, cellular swelling.
Reversible/ Early Ischemic Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
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Cell injury with loss of nuclei, cellular fragmentation and leakage of cellular contents.
Irreversible/ Necrotic cellular injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
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These are chemical species with a single unpaired electron in the outer orbital.
Free radicals(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
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Most common cause of cell injury in clinical medicine.
Ischemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
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Composed of membrane-bound vesicles of cytosol and organelles seen in programmed-cell death.
Apoptotic Bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.19
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Restoration of blood flow to ischemic but otherwise viable tissue paradoxically results in exacerbated and accelerated injury.
Ischemia-Reperfusion Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
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Pathway of apoptosis trigerred by loss of survival signals, DNA damage and accumulation of misfolded proteins. Inhibited by Anti-apoptotic members of the Bcl family.
Mitochondrial / Intrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22
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Pathway of apoptosis responsible for elimination of self-reactive lymphocytes and damage by cytotoxic T lymphocytes. Initiated by TNF receptors.
Death Receptor / Extrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22
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Refers to any abnormal accumulation of triglycerides within parenchymal cells. Most often seen in the liver but can also occur in the heart, sk m., and kidneys.
Fatty Change(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23
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Other name for macrophages in contact with lipid debris of necrotic cells or abnormal forms of lipoproteins. Filled with minute, membrane-bound vacuoles of lipid, imparting a foamy appearance to their cytoplasm.
Foam cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24