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Path 1
Cell Injury, Adaptation, and Death
| Question | Answer |
|---|---|
| Why does hypoxia result in injury | loss of ATP, release of Calcium, and switch to anaerobic glycolysis |
| When Ca++ is released it activates what two enzymes | phospholipase and protease (both result in injury to the cell membrane and chromatin) |
| What is reperfusion injury | damage and/or death of cells after resumption of blood flow to ischemic tissues |
| Why does reperfusion result in injury | increased free radical formation, high Ca++, cytokine production |
| What are reactive oxygen species | atoms or molecules with unpaired electrons |
| 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 |
| how are antioxidants inactivated | Antioxidants (VitE, glutathione, transferrin, ascorbic acid, ceruloplasmin) and Superoxide dismutase; Catalase |
| how do radicals injure cells | lipid peroxidation, cross linking proteins, damage to DNA |
| What is the disease associated with rapid acceleration of aging | Werner's (chromosome 8) google a picture |
| Major change with pyknosis | condensation of nuclear chromatin and reduction in nuclear size |
| Major change with karyolysis | dissolution of the nucleus |
| Major change with karyorrhexis | fragmentation of the nucleus |
| Cell death resulting from severe environmental insult and not from natural intrinsic processes of the cell is known as? | necrosis (not apoptosis) |
| Heterolysis is what? | when enzymes released from inflammatory cells assist in the digestion of necrotic cells |
| Autolysis is what? | autolysis is after cell death and is secondary to the release of proteolytic hydrolytic enzymes from lysozymes within the dead cell |
| Where could you possible see coagulation necrosis | in the heart and lungs |
| Where could you possibly see liquefaction necrosis | brain infarcts and abscesses |
| Where would you be likely to see caseous necrosis | tuberculosis |
| where would you possibly see fat necrosis | peripancreatic mesenteric fat |
| gangrene is another word for? | necrosis |
| Dry gangrene is what type of necrosis | coagulative necrosis |
| Wet gangrene is what type of necrosis | liquefaction necrosis |
| "programmed" cell death is also known as? | apoptosis |
| A baby born with webbed fingers may have had a failure in this process | apoptosis |
| which process is associated with inflammation apoptosis or necrosis | necrosis |
| Is Apoptosis associated with karyolysis or karyohexis | karyorhexis (dense condensed, and fragmented chromatin) |
| is necrosis associated with karyolysis or karyorhexis | karyolysis (illdefined clumping) |
| Atrophy | decreased size and function |
| Hypertrophy | increase in cell size with an increase in organ size and augmented functional capacity |
| Hyperplasia | increase in the number of cells |
| Metaplasia | the reversible conversion of one differentiated cell type to another |
| Accumulation of water results in the tissue results in | edema |
| accumulation of cholesterol in the tissue results in? | xanthoma and atherosclerosis |
| accumulation of copper in the tissue results in? | Wilson's disease |
| accumulation of anthracosis in the tissue results in? | black lung |
| accumulation of bilirubin in the tissue results in? | jaundice |
| accumulation of urate in the tissue results in? | Gout |
| Fas ligand is a suppressor or inducer of apoptosis? | inducer |
| CSF (colony stimulating factor) is a suppressor or inducer of apoptosis? | suppressor |
| TNF and TGF are suppressors or inducers of apoptosis? | inducer |
| Nerve growth factor is a suppressor or inducer of apoptosis? | suppressor |
| Caspases are inducers or suppressors of apoptosis? | inducers |
| bcl-2 is a suppressor or inducer of apoptosis? | suppressor |
| EBV is an inducer or suppressor of apoptosis? | suppressor |
| p53 is an inducer or suppressor of apoptosis? | inducer |
| bax is an inducer or | inducer |
Created by:
UVAPATH1
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