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Flashcards in Cellular Injury and Adaptation Deck (174)
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1

Homeostasis

balance of physiologic and biochemical functions within the body

2

Alteration of homeostasis results in

stress to cell, cellular injury or adaptive changes to survive altered environment

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Reversible injury

injury is corrected prior to destruction of cellular repair mechanisms; severity of injury does not exceed the cells ability to repair itself

4

Irreversible injury

repair mechanisms are destroyed (removal from altered environment will be insufficient) cell cannot repair itself --> DEATH; injury exceeds the cell's ability for self-repair, resulting in cell death

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Cellular Injury

Hypoxia, Physical agents, chemicals, infectious agents, immune reactions, genetic derangements, nutritional imbalance

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Hypoxia

Decreased supply of O2 to cell or inability to use O2

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Anoxia

Complete absence of O2

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Causes of Hypoxia

Ischemia (decreased BF), decreased oxygenation of blood, decreased O2 carrying capacity, inability to utilize O2

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Examples of Physical injury to cell

mechanical trauma, temperature extremes, atmospheric pressure variation, radiation, electrical injury

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Examples of Chemical Injury to cell

Simple agents (electrolytes, glucose), Poisons, Pollutants, Insecticides, herbicides, industrial products, drugs (therapeutic or recreational), alcohol

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Infectious Causes of cell injury

bacteria, rickettsia, fungi, virus, parasite

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Immune Response Causes of cell injury

Hypersensitivity reaction

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4 Key Signs of REVERSIBLE cell injury

Decreased aerobic respiration, cellular edema, ribosome detachment from RER, ultrastructural morphological changes

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Reversible Injury - Decreased Aerobic Respiration Results in

Decreased ATP production, increased AMP and anaerobic glycolysis, Increased lactate (decreased pH), decreased cellular glycogen, clumping of nuclear chromatin, decreased protein synthesis

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Examples of nutritional variations that cause cellular injury

deficits, excess, malabsorption, altered use

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Sites that are altered in cellular injury

cell membrane integrity, aerobic respiration, enzyme/protein synthesis, genetic apparatus

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What causes cellular edema in reversible cell injury?

Suppression of Na+ pump with increased [Na+] retention; increased intracellular Na+

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Ultrastructural Morphological Changes in reversible cellular injury

Phospholipid membrane alteration, loss of microvilli, myelin figure formation, mitochondrial swelling, RER swelling

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Key Signs of IRREVERSIBLE cellular injury

ATP Depletion, Cell Membrane Damage

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Cell Membrane Damage as a result of irreversible damage

Phospholipid Depletion, Cytoskeletal breakdown, toxic ROS, Lipid breakdown products, amino acid loss

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Structural changes in IRREVERSIBLE cell injury include

vacuolization of mitochondria, PM damage, Lysosomal swelling, Loss of proteins, enzymes, and RNA

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What characterizes cell injure as irreversible?

ATP depletion, cellular edema -> PM tears and damage, mitochondrial dysfunction (high [Ca2+] intracellularly), Membrane phospholipid depletion, cytoskeleton changes, ROS, lipid breakdown products, and amino acid loss

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Irreversible Cellular Damage - What is the determining/most important factor?

Cellular Membrane Dysfunction

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Irreversible Cellular Damage - What results from mitochondrial dysfunction?

ATP depletion -> increased cytosolic [Ca2+] -> mitochondrial phospholipase activation -> phospholipid breakdown + accumulation of FFA -> altered permeability of PM

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Myelin figures are characteristic of

reversible injury

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cellular edema is characteristic of

reversible injury

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Irreversible Cellular Damage - What causes membrane phospholipid depletion?

increase [Ca2+] intracellular activation of phospholipase AND ATP-dependent maintenance and production of phospholipids

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Irreversible Cellular Damage - What causes cytoskeletal abnormalities?

Hypoxia AND activation of proteases by high intracellular levels of [Ca2+]

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Irreversible Cellular Damage - What causes Toxic oxygen radical production?

sudden repercussion of hypoxic tissue

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Irreversible Cellular Damage - What produces Toxic oxygen radicals?

segmented neutrophils