Cell Injury, Adaptation, and Death
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| Why does hypoxia result in injury | loss of ATP, release of Calcium, and switch to anaerobic glycolysis
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| When Ca++ is released it activates what two enzymes | phospholipase and protease (both result in injury to the cell membrane and chromatin)
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| What is reperfusion injury | damage and/or death of cells after resumption of blood flow to ischemic tissues
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| Why does reperfusion result in injury | increased free radical formation, high Ca++, cytokine production
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| What are reactive oxygen species | atoms or molecules with unpaired electrons
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| How are reactive oxygen species produced? | High energy sources (x-ray, uv light), Oxidation-reduction reactions (iron and copper) enzymatic metabolism, and cytochrome p450, and xanthine oxidase
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| how are antioxidants inactivated | Antioxidants (VitE, glutathione, transferrin, ascorbic acid, ceruloplasmin) and Superoxide dismutase; Catalase
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| how do radicals injure cells | lipid peroxidation, cross linking proteins, damage to DNA
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| What is the disease associated with rapid acceleration of aging | Werner's (chromosome 8) google a picture
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| Major change with pyknosis | condensation of nuclear chromatin and reduction in nuclear size
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| Major change with karyolysis | dissolution of the nucleus
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| Major change with karyorrhexis | fragmentation of the nucleus
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| Cell death resulting from severe environmental insult and not from natural intrinsic processes of the cell is known as? | necrosis (not apoptosis)
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| Heterolysis is what? | when enzymes released from inflammatory cells assist in the digestion of necrotic cells
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| Autolysis is what? | autolysis is after cell death and is secondary to the release of proteolytic hydrolytic enzymes from lysozymes within the dead cell
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| Where could you possible see coagulation necrosis | in the heart and lungs
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| Where could you possibly see liquefaction necrosis | brain infarcts and abscesses
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| Where would you be likely to see caseous necrosis | tuberculosis
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| where would you possibly see fat necrosis | peripancreatic mesenteric fat
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| gangrene is another word for? | necrosis
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| Dry gangrene is what type of necrosis | coagulative necrosis
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| Wet gangrene is what type of necrosis | liquefaction necrosis
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| "programmed" cell death is also known as? | apoptosis
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| A baby born with webbed fingers may have had a failure in this process | apoptosis
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| which process is associated with inflammation apoptosis or necrosis | necrosis
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| Is Apoptosis associated with karyolysis or karyohexis | karyorhexis (dense condensed, and fragmented chromatin)
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| is necrosis associated with karyolysis or karyorhexis | karyolysis (illdefined clumping)
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| Atrophy | decreased size and function
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| Hypertrophy | increase in cell size with an increase in organ size and augmented functional capacity
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| Hyperplasia | increase in the number of cells
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| Metaplasia | the reversible conversion of one differentiated cell type to another
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| Accumulation of water results in the tissue results in | edema
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| accumulation of cholesterol in the tissue results in? | xanthoma and atherosclerosis
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| accumulation of copper in the tissue results in? | Wilson's disease
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| accumulation of anthracosis in the tissue results in? | black lung
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| accumulation of bilirubin in the tissue results in? | jaundice
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| accumulation of urate in the tissue results in? | Gout
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| Fas ligand is a suppressor or inducer of apoptosis? | inducer
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| CSF (colony stimulating factor) is a suppressor or inducer of apoptosis? | suppressor
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| TNF and TGF are suppressors or inducers of apoptosis? | inducer
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| Nerve growth factor is a suppressor or inducer of apoptosis? | suppressor
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| Caspases are inducers or suppressors of apoptosis? | inducers
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| bcl-2 is a suppressor or inducer of apoptosis? | suppressor
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| EBV is an inducer or suppressor of apoptosis? | suppressor
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| p53 is an inducer or suppressor of apoptosis? | inducer
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| bax is an inducer or | inducer
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