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Fun Path, Unit 1 - 1 Fundamentals of Pathology Unit 1 Study...

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1 Fundamentals of Pathology Unit 1 Study Guide Chapter 1: Cell Injury, Death, and Adaptation: Cellular responses to stress: -- depends on type of cell and type of stress normal cell – homeostasis adaptation – atrophy – decreased cell size protein synthesis affected hypertrophy – increased cell size protein synthesis affected hyperplasia – increased number of cells nervous tissue – unable to reproduce metaplasia reversible injury irreversible injury – cell death Patterns of Cell Death: occurs in cells as they die – irreversible necrosis – coagulative – not in CNS but everywhere else decreased pH pH denatures enzymes denaturation disruption of H+ bonds tertiary structure rupture most proteins globular (enzymes) collagen if fibrillar liquefactive – CNS or infection with gangrene – bacteria have proteolytic enzymes proteolysis brain is sensitive to liquefaction glial cells and neurons rich source of proteases lack of connective tissue apoptosis – programmed cell death can be normal physiology WBC uterine lining fetal development (webbing) can be pathology leukemia – loss of apoptosis Causes of Cell Injury: hypoxia/ischemia chemicals/drugs immunologic reactions nutritional imbalances physical agents microbiologic agents genetic defects aging – free radicals
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2 Mechanisms of Cell Injury: reaction of a cell to an injurious agent is dependent on a number of factors: type of injury, duration, and severity type of cell, physiologic status, adaptability major cellular targets for injurious agents: cell membrane integrity aerobic respiration protein synthesis genetic machinery role of oxygen derived free radicals and loss of calcium homeostasis Ischemic/Hypoxic Injury: reversible injury: mild injury, short duration, cells with protective mechanisms reduced oxygen availability leads to decreased ATP generation reduction ATP synthesis affects: NA/K pump – acute cellular swelling (hydropic change) primary active osmotic regulator uses ~ 1/3 of all ATP produced glycogen depletion – decreased intracellular pH from lactic acid denaturation ribosome detachment – reduced protein synthesis no way to repair self cytoskeletal disruption irreversible injury: continuation of cell stress leads to changes that are not repairable mitochondrial disruption – swelling of organelles from decreased ATP production plasma membrane disruption and calcium influx key change in cell death – increased membrane permeability to calcium – metabolic chaos calcium function: muscle contraction neurotransmitters intercellular communication with second messenger systems release of lysosomal hydrolases isotonic solution RBC no change hypotonic solution RBC swells
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