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13 Cards in this Set
- Front
- Back
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Coagulation Necrosis
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Look like white, firm regions. Cells have lost their nuclei but maintain general appearance and are eosinophilic (red is dead). Called coagulation because proteins become denatured and coagulate (like egg white). Caused by hypoxia.
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Liquefactive Necrosis
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Caused by a localized (focal) infection. Bacteria are attacked by inflammatory cells (primarily neutrophils) that digest the tissue, leaving it filled with puss like structure called an abscess. Microscopically is appears as empty space filled with inflammatory cells.
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Fat Necrosis
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Cause by damage of adipocytes. This is most attributed to pancreatitis where pancreatic enzymes spill out and attack surrounding fat or from trauma. It will appear as a white, chalky tissue due to trigylcerides reacting with Ca++ to form "soaps".
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Caseous Necrosis
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Caused by a local infection where the tissue has walled off the infected area, called a granuloma. It appears as a white, soft, cheesy structure, caused by chronic inflammation from infectious such as TB and Valley Fever. Microscopically cells lack nuclei and look pink
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Fibrinoid Necrosis
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A rare type of necrosis where damaged blood vessels become very stiff and surrounded by fibrin cartilage.
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Gangrenous Necrosis
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Gangrenous necrosis is caused by ischemia (totally blood deprivation) in the lower extremities from chronic cold exposure or circulatory issues as in diabetes II. It can present more coagulative if there is no infection, or liquefactive if there is infection
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Summarize the molecular changes occurring in cells exposed to hypoxia
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Na/K ATP pumps shut down, causing cells to swell.
Ribosomes will break apart and lipids broken down by proteases will accumulate. Nuclear chromatin will unravel due to lactic acid accumulation. |
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Irreversible cell damage (M&M)
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Mitochondria and Membrane damage. Includes swelling, rupture, and fragmentation.
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How does cyanide injure cells?
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Cyanide covalently binds with complex IV (cytochrome oxidase) of the ETC, causing it to back up and lose oxidative phosphorylation ability, cutting off the cells primary ATP source. Just 100mg can be lethal.
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Explain why N-acetylcysteine is used to treat acetaminophen poisoning.
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N-acetylcysteine (NAC) is a precursor to GSH (glutathione) which is the main antioxidant. NAC supplementation produces more GSH which neutralizes and conjugates the free radicals.
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How does an acetaminophen overdose cause damage?
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95% of acetaminophen is detoxified, but the other 5% gives rise to free radicals in the form of NAPQ. Free radicals damage cells in a number of ways.
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Describe the function of the p53 gene.
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A gene activated (part of extrinsic path) when the cell is signaled for apoptosis. Mutations can give cell ability to resist apoptotic signals.
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Describe the function of Bcl-2
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Stands for "B Cell Lymphoma". Inhibitor of cancer cell death by preventing release of apoptotic proteins from mitochondria. Over-expression causes resistance to apoptosis, caused by a 14;18 translocation.
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