| Term 
 | Definition 
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        | Term 
 
        | mechanism of disease development |  | Definition 
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        | Term 
 
        | cell & organ changes due to disease, molecular & genetic changes |  | Definition 
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        | Term 
 
        | functional consequence, sign & sx |  | Definition 
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        | Term 
 
        | 5 options of cell response to injury |  | Definition 
 
        | adaptation, acute reversible injury, irreversible injury/cell death, metabolic changes, cellular aging |  | 
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        | Term 
 
        | describe the 4 ways a cell can adapt to an injury |  | Definition 
 
        | hyperplasia, hypertrophy, atrophy, metaplasia |  | 
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        | Term 
 
        | describe the two ways a cell can die |  | Definition 
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        | Term 
 
        | describe what metabolic changes can occur in a cell after injury |  | Definition 
 
        | intracellular accumulations (proteins, lipids, carbohydrates), calcifications |  | 
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        | Term 
 
        | physiologic v. pathogenic |  | Definition 
 
        | physiologic is a good change, pathologic is a bad change |  | 
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        | Term 
 
        | increase in size of cells or organ |  | Definition 
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        | Term 
 
        | why does hypertrophy happen |  | Definition 
 
        | increased synthesis of structural components or organelles (ex. glycoproteins) |  | 
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        | Term 
 
        | increased muscle mass by pumping iron is an example of what |  | Definition 
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        | Term 
 
        | increased heart size because of hypertension is an example of what |  | Definition 
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        | Term 
 
        | can a cell adaptation be pathologic? Give ex |  | Definition 
 
        | yes! Enlarged heart from hypertension |  | 
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        | Term 
 
        | increase in number of cells |  | Definition 
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        | Term 
 
        | uterus growing in pregnancy is an example of what |  | Definition 
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        | Term 
 
        | liver regenerating after partial resection is an example of what |  | Definition 
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        | Term 
 
        | give an ex of pathologic hyperplasia |  | Definition 
 
        | endometrial, benign prostatic - because it increases risk of malignancy |  | 
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        | Term 
 
        | decreased size or number of cells or organ |  | Definition 
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        | Term 
 
        | why does atrophy happen? 6 reasons. |  | Definition 
 
        | disuse, loss of innervation, loss of blood supply/nutrients, loss of endocrine stimulation (breast, uterus), aging, pressure atrophy |  | 
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        | Term 
 
        | breast and uterine shrinkage in postmenapausal women is an example of what |  | Definition 
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        | Term 
 | Definition 
 
        | yes; cells have diminished function and may progress ot irreversible injury |  | 
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        | Term 
 
        | reversible change of one cell type to another (aka reprogramming of stem cells) |  | Definition 
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        | Term 
 
        | give examples of metaplasia |  | Definition 
 
        | respiratory epithelium to squamous from smoking; squamous to columnar form acid reflux |  | 
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        | Term 
 | Definition 
 
        | protection, but it really raises the risk of cancer |  | 
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        | Term 
 
        | name the 3 kinds of reversible injury |  | Definition 
 
        | decreased oxidative phosphorylation, decreased ATP, morphology change |  | 
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        | Term 
 
        | name two kinds of morphology change due to reversible injury |  | Definition 
 
        | cell swelling, fatty change |  | 
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        | Term 
 | Definition 
 
        | hypoxia, physical agents, chemicals & drugs, infectious agents, immunologic reactions, genetic defects, nutrition |  | 
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        | Term 
 
        | name the 4 things that happen to every cell in reversible injury in order. |  | Definition 
 
        | biochemical alterations, ultrastructural changes, light icroscopic changes, gross morphological changes |  | 
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        | Term 
 
        | inflammation: necrosis or apoptosis |  | Definition 
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        | Term 
 
        | apoptosis and necrosis: pathologic or physiologic? |  | Definition 
 
        | apoptosis can be either; necrosis is always pathologic |  | 
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        | Term 
 
        | how many cells in apoptosis or necrosis? |  | Definition 
 
        | apoptosis is one, necrosis is many |  | 
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        | Term 
 
        | describe the nuclear changes in necrosis. |  | Definition 
 
        | pyknosis, karyorrhexis, karolysis |  | 
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        | Term 
 
        | describe the nuclear changes in apoptosis |  | Definition 
 
        | nuclear/cytoplasmic fragmentation |  | 
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        | Term 
 | Definition 
 
        | used in apoptosis to degrade things |  | 
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        | Term 
 
        | cell death that releases IL-1 |  | Definition 
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        | Term 
 
        | capsase-independent programmed death of many cells |  | Definition 
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        | Term 
 
        | amorphous/flocculent densities |  | Definition 
 
        | marker of mitochondrial damage that means irreversible damage |  | 
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        | Term 
 
        | two markers of irreversible injury |  | Definition 
 
        | amorphous/flocculent densities; loss of membrane functions; mitochondrial dysfunction |  | 
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        | Term 
 
        | different kinds of necrosis |  | Definition 
 
        | coagulation, liqueifactive, caseation, fat, fibrinoid necrosis |  | 
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        | Term 
 
        | what properties of cell injury depend on the injury? |  | Definition 
 
        | injury, duration, severity |  | 
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        | Term 
 
        | what properties of cell injury depend on the cell that is injured? |  | Definition 
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        | Term 
 
        | 6 mechanisms of cell injury |  | Definition 
 
        | ATP depletion, mitochondrial damage, increased Ca, free radical damage, membrane damage, DNA damage |  | 
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        | Term 
 
        | How does loss of ATP depletion lead to cell injury? |  | Definition 
 
        | loss of oxidative phosphorylation, so intracellular pH decreases, Na pump stops functioning, Ca pump fails, no protein synthesis |  | 
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        | Term 
 
        | how does mitochondrial damage lead to cell injury? |  | Definition 
 
        | membrane permeability of mitochondria means no ATP and leakeage of cytochrome c into the cytosol |  | 
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        | Term 
 
        | how does increased Ca lead to cell injury? |  | Definition 
 
        | activates destructive enzymes |  | 
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        | Term 
 
        | how does free radical damage lead to cell injury? |  | Definition 
 
        | oxidative stress: lipid peroxidation, enzyme damage, nuclear damage |  | 
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        | Term 
 
        | how does a membrane get damaged? |  | Definition 
 
        | ATP depletion, free radicals, decreased phospholipid synthesis (or increased breakdown), cytoskeletal abnormalities |  | 
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        | Term 
 
        | loss of osmotic balance, Ca+ influx, leakage of enzymes: what is damaged? |  | Definition 
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        | Term 
 
        | decreased ATP: what is damaged? |  | Definition 
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        | Term 
 
        | how does DNA damage occur |  | Definition 
 
        | radiation, drugs, oxidative stress |  | 
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        | Term 
 
        | what happens following dna damage |  | Definition 
 
        | repair mechanisms are overwhelmed and apoptosis is initiated |  | 
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        | Term 
 
        | where do intracellular accumulations come from? |  | Definition 
 
        | endogenous in excess or abnormal, exo (coal, tattoo) or endo (lipids, etc.) - can be harmless or toxic |  | 
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        | Term 
 
        | ex of intracellular accumulations with bad outcomes |  | Definition 
 
        | fatty liver (too many triglycerides), smokers |  | 
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        | Term 
 | Definition 
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        | Term 
 | Definition 
 
        | heart cells tat have wear & tear injury from free radicals; doesn't affect function of cells |  | 
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        | Term 
 | Definition 
 
        | in liver - golden deposits that affect function (cirrhosis) |  | 
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        | Term 
 
        | a normal process in dying or dead tissues calcification |  | Definition 
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        | Term 
 
        | hypercalcemia in normal tissues |  | Definition 
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        | Term 
 
        | mechanisms behind cell aging |  | Definition 
 
        | telomere shortening, oxidation, failure of repair mechanisms, lipofuscion from peroxidation |  | 
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