2 cell injury, adaptation, & death

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Cell Injury, Adaptation, & Death

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Cell Injury, Adaptation, & Death

Cell Injury, Adaptation, & Death

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CellsTissues

OrgansSystemsOrganism

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How is meiosis different?

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Tumor suppressor genessynthesize growth inhibition proteinsp53Proto-oncogenesstimulate cell growth

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Proliferation of CellsLabilecontinuous reproductionStablereproduce slowly until injuredPermanentno division

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Biologic AgingApoptosisProgrammed cell deathNecrosisDeath caused by diseaseAs cells age, functioning decreasesGenetically, telomeres influence cell aging

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All disease occurs because of cell injuryEither because of the injury itself or the repair process that follows

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Causes of Cell InjuryHypoxia

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HypoxiaInadequate oxygenationMost common cause of cell injuryUsually due to ischemiaCauses chemical & acid-base imbalancesReversible if O2 restored or death if not

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Causes of Cell InjuryHypoxiaDirect physical action

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Direct Physical Action

Major problems are hemorrhage & ischemia

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Causes of Cell InjuryHypoxiaDirect physical actionIonizing radiation

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Ionizing RadiationIonizes H2O into H+ & OH-OH- attaches to DNA & prevents cell reproductionDNA mutations

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Causes of Cell InjuryHypoxiaDirect physical actionIonizing radiationToxic molecular injury

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Toxic Molecular Injury

Dose related

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Causes of Cell InjuryHypoxiaDirect physical actionIonizing radiationToxic molecular injuryMicrobes

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MicrobesToxins can interfere with protein synthesis or utilization of O2

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Causes of Cell InjuryHypoxiaDirect physical actionIonizing radiationToxic molecular injuryMicrobesInflammatory & immune reactions

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Inflammatory & Immune ReactionsDue to cell injury & then in turn causes injury

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Causes of Cell InjuryHypoxiaDirect physical actionIonizing radiationToxic molecular injuryMicrobesInflammatory & immune reactionsNutritional imbalancesGenetic defectsAging

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Mild Cell InjuryHydropic changeNa/K pump damaged so Na+ increases in the cell & H2O moves in causing swelling

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Intracellular AccumulationsSome due to phagocytosis or other normal physiologic mechanisms

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Fat

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CholesterolMost extensive & damaging accumulationAtherosclerosis

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Protein

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Glycogen

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Pigments

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Adaptations

Change in sizeChange in number of cellsChange into another type of cell

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AtrophyDecreased size & functionMetabolic processes shut down to conserve energyDue todecreased demandischemialack of nerve or hormonal stimulationchronic inflammation

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HypertrophyIncreased size & functional capacityDue tohormonal stimulationincreased functional demand

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HyperplasiaIncrease in number of cellsDue tohormonal stimulationincreased functional demandchronic stress or injury

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DysplasiaDisorderly overgrowth of cellsPremalignantReversible

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MetaplasiaOne cell type to anotherReversible

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NecrosisPathologic cell deathUsually in a collection of cells fed by a single artery

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Coagulative NecrosisMost commonDead cells form a gel-like consistencyNo anatomic disruption so cells or tissues are left with a ghostly outlineInfarction most common cause

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Liquefactive NecrosisDead tissue dissolves into liquidDead cells disrupted faster than it can be cleaned up

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Caseous NecrosisTBcheesyCellular detail gone

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Fat NecrosisMay due to traumaTriglycerides digested & free fatty acids precipitate as calcium saltsOne type of dystrophic calcification

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GangreneDrypart is dry & shrinksskin wrinklesdark brown or blackslow spreadline of demarcationform of coagulation necrosisextremitiesWet (moist)part cold, swollen, pulselessmoist, black, & under tensionliquefaction occursfoul odorno line of demarcationspreads rapidlydeath if not stoppedorgans & extremities

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