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71 Cards in this Set
- Front
- Back
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1) Adaptations to persistent stress |
Hypertrophy
Atrophy hyperplasia metaplasia: reversible, change of cell type dysplasia: precancer, microscopic |
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2) Cells that undergo Hypertrophy |
Happens in cells that cant divide: -skeletal muscle -cardiac muscle -myometrium (uterine wall) |
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Cardiac morphology -Cardiac hypertrophy happens bc of __ in response to _ -maks increase in _ of hrt and _ of ventricular wall. makes _, _ nuclei |
-increased work load on response to hypertension -weight of hrt and thickness of ventricular wall. -makes boxy enlarged nuclei |
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3) Cells that adapt via hyperplasia Epithelial: |
-skin -linings of everything tube like esophagus, intestine, gland ducts, plus glands and liver |
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Hormone-related: |
-endometrium, brst ducts -prostate gland -adrenal gland, thyroid gland |
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Growth factor related: |
-liver regeneration after removal of a part of it -warts and HPV -keloid -psoriasis |
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4) What adaptive changes happen in fat cells? |
-hyperplasia in children (increase in number until pubrty) -hyperTROPHY w weight gain in adults -atropohy w weight loss in both |
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5) Atrophy is decrease in __ Most common cause: Other causes of atrophy: |
-cell size and number -aging (brain, liver, kidney, muscle, bone) -disuse (cast) -loss of endocrine (lose endometrium and breast tissue) -denervation (polio, severed nerve) -diminished bld suply from atherosclerosis (brain, renal) -pressure atrophy (mass lesion, ulcer) -inadequate nutrition (marasmus, muscle loss thru autophagy, cancer cachexia) |
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6)Outcomes of atrophy: -cell can _ or _ from ___ |
cell may recover or could die from apoptosis or autophagy (self eating) |
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7) what is metaplasia? |
-reversible change -of adult cell to another type of adult cell -to different phenotype |
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3 types of metaplasia: |
-squamous -columnar -dysplasia? |
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Squamous metaplasia-> most common -happens when __ change to __ -ex: |
-columnar or cuboidal change into squamous -ex: columnar become squamous on lung epithelium from smoking |
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Columnar metaplasia: -change from _ into _ ex: |
-change from squamous into columnar/glandular epithelium ex: from irritation of acid reflux into distal esophagus |
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When irritation is persistent or prolonged, __ can develop |
dysplasia precancer |
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2 major types of cell death: are they pathogenic? |
necrosis ALWAYS PATHOGENIC apoptosis can be PATHO or PHYSIO |
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hypoxia is |
no oxygen |
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ischemia is |
no bld flow bc of obstruction |
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Cell injury mechanisms: -depletion of __ -happens bc of hypoxic or ischemic -consequences of ATP loss: -->__pump activity decrease (causes influx of _ and _ INTO cell, cell swels, eflux of _) -->__pump fail, so intracellular __ goes _ |
-ATP -Na (causes influx of Na into, efflux of K out ) -Ca pump fails, so intracell Ca does up! |
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Next, -__detach, so __ is disrupted, so apoprotein production reduced. -intracellular __ accum (fatty change - steatosis) -__ stores deplete so switch to _, which makes __ -unfolded proteins accum, make a response that leads to __ |
-ribosomes detach, so protein synth disrupted -intracell lipid accum -glycogen stores deplete, switch to anaerobic glycolysis, which makes lactic acid -leads to cell death |
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Characteristics and morph of REVERSIBLY injured cells: -__ is depleted -__ is reduced -cell is ____! -___change!:small or large lipid vacuoles in cytoplasm |
-ATP -oxidative phos -SWELLING -FATTY CHANGE |
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Necrosis is ___ injury. -defined as cll death -cells degraded by __ -morphological changes appear hours after __ |
irreversible -degraded by lysosomal enzymes -after death |
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morphology of necrosis: -increased __ of cytoplasm -__ appearance -__ (looks moth eaten) -dead cells can undergo __ -nucleus changes: -->karyolysis: -->pyknosis: -->karyorhexis: |
-eosinophila (more pink) -homogenous -vacuolated -calcification --->fading of nucleus --->nucleus small and compact --->fragmented nucleus |
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13) Mitochondrial injury has two outcomes: -__ via loss of __ -__ via release of __ |
-necrosis via loss of ATP -apoptosis via release of cytochrome c |
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14) intracellular Ca __ during cell injury -leads to increase in activity of _ -leads to cell destruction bc some of them destroy membrane, proteases lyse cytoskeleton and endonucleases digest nucleus |
-increases -leads to increase enzyme activity |
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15) Free radicals are: -include ROS, super_, hydr perox, and __radicals, nitric__metabolites, and other electrophilc compounds. -includes the metabolites of __ and __ |
-superoxide, hydroxyl radicals, nitric oxide metabolites, -metabolites of carbon tetrachloride and acetominophen |
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16) sources of free radicals: -__toxicity -normal __ -nitric __ -inflamm/__ -transition metal reactions (iron, copper) -exogenous chems like drugs, ethanol |
-oxygen toxicity -normal metabolism -nitric oxide -infection |
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hydroxyl radicals come from |
-radiation and Fenton rn |
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Fenton rn: -makes __ from __ in presence of __ |
makes hydroxyl from hydrogen peroxide in presence of ferrous ions |
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acetominophen/tylenol overdose results in __ in __. -can overwhelm s__, and g__, lead to massive ____ |
free radical metabolite formed in liver. -can overwhelm scavenger and glutathione -lead to masive hepatocyte necrosis |
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17) pathological effects of free rads -__dmg -brk down, misfold of __ -dmg to __ (mutations) |
-membrane dmg -misfold of proteins -DNA dmg mutations |
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18) factors for removal of free radicals -free rad scavengers includes: __, cata_, superoxide _, vits _, _ bound to protein, copper bound to _ |
-glutathione -catalase -superoxide dismutase -vits A E C -iron bound to protein -copper bound to ceruloplasmin |
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how it works is -superoxide converted to __ by __ -then __ decomposed into water by __ and __ |
-h2o2 by SOD -then h2o2 convert to water by glutathione and catalase |
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20) effects of ROS on membrane dmg: -lipid ___ from free rads -depleted __ and higher __ -cell death (releases contents, can measure in blood) |
-lipid peroxidatino -depleted ATP, higher Ca |
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21) misfolded proteins leads to __ -they accum with age, dereasing __, -result is __ |
-apoptosis! -decreasing cell fncn -results is lots of degenerative diseases related to aging |
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21) Patterns of Necrosis: - - - - - |
-coagulative -liquefactive -gangrenous -caseous -fat |
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Coagulative necrosis -happens with __ -ex: _ -tissue stays _ -cell outlines are _ -those dead cells removed by _ |
-ischemic, hypoxic -myocardial infarction -firm -preserved -phagocytosis |
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Coagulative at microscopic level: -lots of purple dots -neutrophils and eosinophils -fragmentation karyorrhexis and karyolysis |
. |
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for renal infarction, looks like |
-tissue turned yellow there |
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Liquefactive necrosis -tissue _ -stroke or _ of abcess -outlines are _ -tissue does mushy |
-dissolved -center -lost see pics |
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Caseous necrosis -NEEDS ___ with giant cells -and epithelial __ -makes white cheesy area -is the response to _ |
-GRANULOMAS -and epithelioid macrophages -tuberculosis |
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Fat necrosis -2 types: _ and _ -traume ex: -enzymatic ex: -little white clumps |
-traumatic and enzymatic -any fat, common in breast fat -lipase, panc enzyme released into ab in acute pancreatitis |
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Gangrenous necrosis -not distinctive -usually _ mixed with _ -gangene of legs can be wet or dry Wet: -_ with _, usually seeen in _ Dry: -no _, tissue _ |
-ischemia mixed with infection -wet is ischemis and infection, seen in diabetics -dry is no infection and tissue mummafied |
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22) types of cell death: -_ -programmed cell death: (3 of them) |
-necrosis -apoptosis, necroptosis, pyroptosis |
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Necrosis vs apoptosis -Cell size: |
-N: swelling -A: reduced (shrinks) |
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-nucleus: |
N: pyknodid, karyorrhexis, karyolysis A: fragmentation into nucleosome-size fragments |
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-plasma membrane |
N:disrupted A: intact but structure altered, esp orientation of lipids |
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-cellular contents |
N: enz digestion, may leak out of cell A: intact, may be released in apoptotic bodies |
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-adj infalmm? |
N: frequent A: no |
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physio or patho: |
N: pathologic (culminatino of IRREVERS cell injury) A: often physio, way to get rid of unwanted cells, could be patho after a cell injury esp DNA dmg |
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23) Pathways of apoptosis -mitochondrial (_) -death receptor (_) |
-intrinsic -extrinsic |
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Extrinsic-death receptor initiated pathway: -receptor-activated __ with death _ -ex: _ligand -elim of _ -think _*** |
-adaptor proteins with death domains -FAS/FAS ligand -elim of autoreactive lymphs -think CASPASES!** |
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Intrinsic-Mitochondrial Pathway: -DNA_ withdrawal _ |
-DNA dmg withdrawal hormones |
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Intrinsic pathway regulators: BCl 2 family Antiapoptosis: BCl2, BClx Proapoptosis: Bax, Bak, Bid -so if no survival signals, and there is DNA dmg, then __ come into play and make cytochrome c leak, activate __, does Apoptosis |
-Bax, Bak or Bid -CASPASES |
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Cytotoxic T-lymphocyte mediated apoptosis -key words are _ and _ (do apoptosis) -important in response to _, immunity against _, transplant rejection, some IV hypersensitivity rns |
-perforins, granzymes -viral infetions, against cancer |
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24) Other forms of programmed cell death: -autophagy -necroptosis: looks like necrosis (with loss of _ and cell_), but is triggered by _. is independent of _. important in cardiac _, and some inflamm diseases -pyroptosis: response to _, cell _, loses plasma membrane and releases IL-1 that causes _. cell activation via _ using caspase 1 |
-ATP, and cell swelling -cardiac reperfusion -response to infection, cell swells, IL-1 causes fever. -cell activation via inflammasome caspase 1 |
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25) Anthracosis: -_accum in _. -ex inhaled in lungs -taken up by _ and retained in lung lymph nodes -no fncn impairment tho |
-carbon accum in intracellular -taken up by macrophages |
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26) Steatosis-fatty change -accum of _ in _ -revers or irrevers? -seen in _ (from obese, diabetes, alcohol, toxins, starvaation) |
-accum of TAGs in intracell -REVERSIBLE -liver |
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Cholest, foam cells -macrophages that took up cholest -common seen in _ -when _ cholest is increased, foamy macrophages accum in _. -can also accum in _ |
-areas of prior injury -serum cholest -accum in xanthomas, xanthelasma (eyelid) -accum in bld vessel walls (atherosclerosis) |
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27) hyaline means |
accum of protein on wall of artery |
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hyaline change: -nonspecific -accum of _ -can be intracell or _ -appearance: ex: extracell would be arteriole walls |
-proteins -intra or extracelluar -homogenous, glassy, pink stain |
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28) Lipofuscin -pigment for _ -yellow brown granules within _ of cells (come from undigested _, _, ceroid) -product of autophagy from ROS -found in organs with _ -seen in _ -no adverse effects though |
-wear and tear -lysosomes, undigested lipids, proteins, ceroid -organs with little turnover like hrt and liver -seen in aging |
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29) Melanin: -made by _ in skin -distributed to protect nuclei from _ -also occurs in _ -amnt determines eye _ |
-melanocytes -UV dmg -eye -eye colour |
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30) Iron accum -_ is small amnt -_ is lots of iron |
-hemosiderin -hemochromatosis |
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-can see using _stain -can be present in _ -accums in lots of tissues including _ in pts with iron overload like sickle cell |
-prussian blue stain -bruises -liver -blue part in pick is iron |
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31) Bilirubin: -comes from brk down of _ (from the heme) -_ is from excess bilirubin -_ describes the sclera and sometimes skin |
-brk down of RBCs -jaundice -icterus |
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32) Dystrophic vs metastatic calcification -serum: |
D: calcium is normal M: too much Ca in bld or too much phosphate |
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-where deposited: |
D: necrosis, all types (esp caseous and fat), atherosclerosis, calcific aortic stenosis, breast tissue M: stomach, kidneys, lungs |
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-causes: |
D: old irreversible injury M: hyperparathyroidism and chronic renal failure |
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33) Factors in cell aging: -cellular _: cell cant divide bc of shortening _ -tumour _ gene product accum -DNA dmg |
-senescence, bc shortening telomeres -tumor suppressor gene product accum |
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-what does lamin do |
-lamin is nuclear organizing protein |
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34) telomeres
-shorten with each _ -when not there, cell is in _ (known as _) -telomerase does what? not found in _ -telomerase found where |
-cell division -not there, cell in terminal nondividing state (replicative senescence) -telomerase puts more telomeres there . not found in somatic cells! |
