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2010-09-02 16:55:19
Pathophysiology Cell Injury Aging Death Chapter Test

Notes for first lecture on Cell Injury, Aging, and Death
Show Answers:

  1. Define Etiology
    The Cause
  2. Define Pathogenesis
    The Development
  3. Define Clinical Manifestations
    The Symptoms
  4. Define Inherited
  5. Define Congenital
    Born with it
  6. Define Metabolic
    Screwed up chemical reactions
  7. Define Degenerative
    tissues/organs progressively degrate over time
  8. Define Neoplastic
    abnormal growth of cells
  9. Define Immunologic
    dealing with the immune system
  10. Define Infectious
    invastion of virus, bacteria, or parasite
  11. Define Physical Agent-Induced
    like altitude, wetness, radiation, lightning, fire
  12. Define Nutritional Deficiency
    nutrients not available
  13. Define Iatrogenic
    due to medical intervention
  14. Define Psychogenic
    mental or emotional connection
  15. Define Idiopathic
    unknown cause
  16. Name Intrinsic Etiologic Factors
    • Inherited
    • Congenital
    • Metabolic
    • Degenerative
    • Neoplastic
    • Immunologic
    • Nutritional Deficiency
    • Psychogenic
  17. Name Inanimate Extrinisic Etiological Factors
    • Physical Agent Induced:
    • Force
    • Temperature
    • Humidity
    • Radiation
    • Electricity
    • Chemicals
  18. Name Animate Extrinisic Etiologic Factors
    • Infectious:
    • Pathogenic organisms
    • Viruses
    • Bacteria
    • Fungi
    • Protozoa
    • Insects
    • Worms
  19. Define Ischemia
    Poor Perfusion or intterrupted blood flow
  20. Describe what happens during Hypoxic Injury
    Lack of oxygen --> ATP deficit --> decrease in ion pump activity --> Na and water accumulate in the cytosol and in organelles --> anaerobic respiration --> acidification --> enzyme dysfunction due to abnormal pH
  21. Describe what happens during Reperfusion Injury
    Ca 2+ ions suddenly become available --> enter cells and activate destructive enzymes that target lipids --> cell contents spill --> local immune cells activated --> Chemokines are released from immune cells --> Neutrophils arrive and release reactive oxygen species --> Inflammation
  22. Define Nutritional Injury
    Lack of essential vitamins and minerals prevents cell funcion and cell division
  23. Define Infectious Injury
    Bacterial enzymes damage host connective tissue and plasma membranes --> bacterial exotoxins interfere with host neuromuscular signals --> Bacterial endotoxins cause inflammation
  24. Define Immunologic Injury
    the immune system is activated by chemicals that are associated with injured host cells and/or infective agents
  25. What is the Etiology of Chemical Injury
    • free radicals that damage
    • antimetabolites interfere with DNA synthesis
    • conversion to toxic compounds
  26. What are Physical and Mechanical Injury
    • Extreme cold
    • extreme heat
    • extreme atmospheric pressure
    • Mechanical deformation --> cell membrane tear, ischemia, blunt force
    • Electric Current --> disrupts neuromuscular signaling, causes burns, causes blood clots
  27. What are the effects of electromagnetic radiation?
    • genetic damage
    • acute cell destruction
  28. How does electromagnetic radiation damage cells
    damage is caused by breaking chemical bonds and by generating free radicals
  29. What is Hydropic Swelling?
    Decreased ATP stalls Na+/K+ pumps --> Na+ accumulates inside cell
  30. What are the characteristics of Hydorpic Swelling?
    • Swelling of cells
    • Large, pale cytoplasm
    • Dilated ER
    • Swollen mitochondria
  31. What is Intracellular Accumulations?
    • excess accumulation of normal stuff (e.g. fat, carbs, glycogen, proteins)
    • OR
    • excess accumulation of abnormal stuff
    • OR
    • excess accumulation of pigments/particles the cell normally would degrade
  32. What is Atrophy?
    Cells become smaller and less active
  33. What causes atrophy?
    • Disuse
    • Lack of nutrients or oxygen
    • Lack of hormonal stimuli
    • Aging
    • Injury due to inflammation or infection
  34. What is Hypertrophy?
    • BIGGER cell
    • may be more active or develop abnormal activities
  35. What is Hyperplasia?
    • MORE cells
    • cells divide more often so more cells then normal are present
  36. What are some examples of Hyperplasia?
    • Caluses
    • Liver cells in the presence of toxins
    • Blood vessel endothelial cells in artherosclerosis
  37. What is Metaplasia?
    One normal cell type change to another cell type

    e.g. ciliated columnar changes to stratified squamous in smoker's bronchi
  38. What is Dysplasia?
    • Normal cells go abnormal but are not yet malignant
    • Abnormal variations in cell shape, size, and arrangement
  39. What are the two types of irreversible cell injury?
    Necrosis and Apoptosis
  40. What is the cause of Necrosis
    Ischemia or toxic injury
  41. What happens during Necrosis?
    cell rupture, contents spill into extracellular space, inflammation
  42. What happens during Apoptosis?
    • cell commits suicide
    • cell in ingested by neighboring cells
  43. What happens during Necrosis?
    high intracellular Ca+2 levels cause activation of destructive enzymes --> internal structures destroyed --> cell contents fine way into bloodstream --> inflammation, malaise, fever, increased heart rate, WBC increased, loss of appetite
  44. What are the four types of Necrosis at the tissue level?
    • Coagulative Necrosis
    • Liquefactive Necrosis
    • Caseous Necrosis
    • Fat Necrosis
  45. What causes Coagulative Necrosis?
    • ischemia
    • deals with denatured proteins and is solid
  46. What causes Liquefactive Necrosis?
    • inschemia in the brain tissue or a bacterial infection in any tissue with WBC involved
    • causes cyst or abscess
  47. What causes Caseous necrosis?
    • mycobacterial infection or tumors
    • debris gets walled off by WBCs
  48. What causes Fat Necrosis?
    • due to injury to fat or pancreatitis
    • causes fatty acid calcium soaps to form
  49. What are the three types of Gangrene?
    Wet, dry, and gas
  50. What is Dry Gangrene?
    large area of coagulative necrosis

    blackened, dry, wrinkled tissue that has clear separation from healthy tissue
  51. What is Wet Gangrene?
    coagulative or liquefactive necrosis followed by infection

    spreads rapidly, releases toxins into bloodstream --> very life threatening
  52. What is Gas Gangrene?
    wet gangrene has been infected with Clostridium perferingens, an anaerobid bacteria

    infections spreads fast thru necrotic tissue
  53. What is the difference between Necrosis and Apoptosis?
    Apoptosis is programmed cell death, no cell contents are spilled, no inflammatory response occurs

    Necrosis involves spillage of cell contents into interstitial space, causes inflammatory response, is alway abnormal
  54. What causes Apoptosis?
    • -loss of survival signals from adjacent cells
    • -delivery of Fas Ligand to activate "death" receptors on plasma membrane
    • -DNA damage with accumulation of protein p53
    • -Intracellular Enzymes and signals
  55. What are the steps of Apoptosis?
    • Activation of caspase enzymes
    • Breakdown of cellular structures
    • Cytoplasmic budding
    • Apoptic bodies released
    • Phagocytosis of apoptotic bodies
  56. What are the theories of Aging?
    • Somatic Mutation Theory
    • Free-Radical Theory
    • Immunologic Theory
    • Error-Prone Theory
    • Neuroendocrine Theory
    • Programmed Senesence Theory
  57. What is the somatic mutation theory?
    DNA damaged by background radiation causes aging
  58. What is the Free Radical Theory?
    Cumulative free radical damage causes aging
  59. What is the Immunologic Theory?
    Autoimmune responses cause aging
  60. What is the Error-Prone Theory?
    Random errors in protein translation causes aging
  61. What is the Neuroendocrine Theory?
    The decline in hormone levels and hormone-receptor sensitivity causes aging
  62. What is the programmed Senescence Theory/
    • Cells undergo a finite number of divisions and then die
    • The telomeres shorten over time
  63. What are the events of Somatic Death?
    • Pallor, dilated pupils, body temperature falls, fluids collect in dependent areas
    • 6 hours later --> rigor mortis
  64. What is rigor mortis?
    accumulation of calcium and depletion of ATP --> prolonged crossbridge formation (can't release muscle contraction)
  65. What is Brain Death?
    • Absence of reflexes
    • Absence of respiratory effort
    • Absence of brain waves
    • Lack of cerebral blood flow
  66. What are Pathophysiologic processes?
    challenges that disrupt normal cell function
  67. How do cells respond to challenges?
    • Cell Adaptation
    • Cell Injury --> Cell Death