Pathophys objective flash cards.txt

Card Set Information

Pathophys objective flash cards.txt
2011-01-30 23:53:44
Pathophys objectives quiz

Pathophys objectives quiz 1
Show Answers:

  1. What are the eight classes of cell injury?
    Oxygen deprivation, Chemical Agents, Infectious agents, Immunologic reactions, genetic defects, genetic imbalances, physical agents, aging
  2. What are three effects of reduced ATP during ischemia/hypoxia?
    ATP-dependent sodium efflux pump cannot function, ATP dependent Calcium cation efflux transport cannot function, anaerobic glycolysis increases as an attempt to restore the ATP levels
  3. What is the effect of decreased function of the ATP dependent sodium efflux pump?
    increased intracellular sodium cations, decreased potassium ion concentration, influx of water, cellular swelling, decreased protein synthesis
  4. What is the effect of decreased function of the ATP dependent calcium cation efflux?
    activation of ATPases, phospholipases, proteases, endonucleases
  5. What is the effect of increased Anaerobic glycolysis?
    decreased glycogen stores, decreased pH level in the cell, decreased activity of cellular enzymes, detachment of ribosomes
  6. How does ROS cause cellular injury?
    functions as oxidizing agents
  7. How does production of OFRs and ROS occur?
    Incomplete reduction of O2 during respiration, Accepting or donating of electrons by transition metals, Absorption of X-rays, Detoxification or metabolism of chemicals in liver, Enzymes involved in inflammatory processes
  8. What does ROS react with?
    Fatty Acids, Proteins, DNA
  9. What removes free radicals?
    SOD, Glutathione peroxidases, catalase
  10. What are the five contexts in which apoptosis occurs?
    depravation of hormones or GF (menstruation), irreparable DNA damage, accumulation of misfolded proteins (alzheimer's), Immune system development, Embryogenesis (loss of vestigial tail)
  11. Hypertrophy
    increase in cell size but not number caused by increase work load, occurs by increased protein synthesis
  12. Hyperplasia
    increase in cell number but not size (breast growth)
  13. Atrophy
    decrease in cell size but not number caused by decreased work load, proteins degrade and protein synthesis decreases
  14. Metaplasia
    one adult cell type is replaced by another
  15. where does fat accumulation occur?
  16. What causes fat accumulation?
    ethanol consumption and diabetes
  17. what is the effect of fat accumulation?
    decreased liver function
  18. what causes lipofuscin accumulation?
    Damage due to ROS or OFR which indicates aging
  19. what causes Hemosiderin accumulation?
    break down of hemoglobin at sites of localized injury or hemmorrhage; associated with systemic overload of iron
  20. What disease causes dystrophic calcification?
    rheumatic heart disease, heart valve becomes sticky causing leakage
  21. what is dystrophic calcification associated with?
    accumulation of Ca associated with necrotic cells
  22. What is metastatic calcification associated with?
    pathologic bone reabsorption
  23. What causes metastatic calcification?
    metastatic cancer
  24. What is the effect of metastatic calcification?
    death of cells of the vasculature, kidneys, lungs, and gastric mucosa
  25. What are the three factors that contribute to cellular aging?
    accumulation of damage (lipofuscin, incorrectly folded proteins/ cross-linked proteins, protein glycosylation, free radical damage), incomplete replication of protein ends by telomerase, reduced regenerative capacity of stem cells
  26. What are the 5 local signs of acute inflammation?
    Heat, redness, swelling, pain, loss of function
  27. What does changes in vascular diameter lead to?
    Vasodilation, increased viscosity, margination
  28. What causes vascular permeability?
    endothelial cell contraction which leads to gaps that leak fluids, direct injury to endothelial cells, leukocyte-dependent endothelial cell damage, increased fluid flow through endothelial cells, leakage from new blood vessels that form at the site of injury
  29. What are the effects of vascular changes?
    release of transudate, release of exudate, edema
  30. What is margination?
    WBC flow along the inner wall of blood cells due to changes in blood flow
  31. What is rolling?
    leukocytes tumble along the wall
  32. What is transmigration?
    leukocyte squeezes through the gaps in edothelial cells
  33. What on endothelial cells binds to sialyl-lewis X-modified glycoprotein on leukocytes to slow down the leukocyte?
  34. What on Leukocytes binds to ICAM-1 and UCAM on endothelial cells to cause firm binding?
  35. What is chemotaxis?
    leukocytes follow a chemoattractant gradient composed of bacterial peptides, complement components, and cytokines to the site of an infection
  36. What receptor on leukocytes do chemoattractants bind?
    7-transmembrane G-protein coupled receptor
  37. What mediates phagocytosis allowing for regulation?
  38. What is a phagosome?
    phagocytic vacuole containing foreign bodies
  39. What destroys the foreign body in the phagosome?
    fusing with a lysosome which contains an oxidative burst
  40. What are examples of circulating mediators of inflammation?
    complement proteins, kinins, and coagulation factors
  41. How are circulating mediators of inflammation activated?
  42. What cells produce histamine?
    mast cells, basophils, and platelets
  43. When is histamine released?
    physical injury, immune reactions, complement binding, neuropeptides, and cytokines
  44. What effect does histamine have?
    arteriolar dialation, increased vascular permeability, endothelial cell contraction; this results in swelling, edema, and congestion
  45. What does COX metabolize AA into?
  46. Lipoxygenases metabolize AA into?
    leukotrienes and lipoxins
  47. What do PGs cause?
    vasodilation and edema; pain and fever
  48. What type of drugs are COX inhibitors?
  49. What do Leukotrienes cause?
    vasoconstriction and increased vascular permeability; airway constriction
  50. What do lipoxins do?
    counteract the activity of leukotrienes
  51. What cleaves Factor XII?
  52. What two systems are triggered by Factor XII activation?
    Kinin system, Complement system
  53. C5b
    triggers assembly of MAC
  54. C3a and C5a
    trigger histamine release
  55. C5a
    chemoattractant for WBC
  56. C3b
    obsonin which aids in phagocytosis
  57. What are the three outcomes of acute inflammation?
    restoration to pre-injury state, scaring or fibrosis, chronic inflammation
  58. What are the three main characteristics of inflammation?
    infiltration by macrophages, lymphocytes and plasma cells, continuous tissue destruction by inflammatory cells, extensive tissue repair including angiogenesis and fibrosis
  59. In what settings do chronic inflammation arise?
    viral infections, persistent microbial infections, prolonged exposure to toxic agents, autoimmune diseases
  60. What role do macrophages play in chronic inflammation?
    release proteases, ROS, factors that release and promote inflammation, angiogenesis factors, growth factors stimulating infiltration and fibrosis
  61. What role do lymphocytes play in chronic inflammation?
    produce mediators which activate macrophages
  62. What role do plasma cells play in chronic inflammation?
    Produce antibodies
  63. What role do eosinophils play in chronic inflammation?
    produce major basic protein which is toxic
  64. What role to Mast cells play in chronic inflammation?
    produce histamine and AA metabolites which play a role in anaphylactic shock and allergic reactions
  65. Labile cells
    permanently dividing and capable of regeneration (skin and GI tract)
  66. Stable Cells
    normally nondividing but can divide in response to injury and regenerate themselves (liver, kidney, pancrease, fibroblastic connective tissue cells, endothelial cells)
  67. Permanent cells
    Non dividing cells that are not capable of regeneration (nerves)
  68. What regulates the cell cycle?
    cyclins binding to CDK which then become active and phorphorylate proteins to begin the cell cycle
  69. Autocrine
    targets the same cell that produced the factor
  70. Paracrine
    targets adjacent cells
  71. synaptic
    specialized form of paracrine signaling
  72. Endocrine signaling
    hormone functions at a site distant
  73. Tyrosine Kinase
    EGF--> EGFR-->RAS-->MAP Kinase Cascade-->cyclin transcription
  74. Interstitial Matrix
    amorphous gel between connective tissue
  75. What is the interstitial matrix composed of?
    collagen, elastin, and proteoglycans
  76. Basement membrane
    sits beneath epithelium to provide support
  77. What is the basement membrane composed of?
    type IV collagen, laminin, other adhesive glycoproteins and proteoglycans
  78. What is the function of the basement membrane?
    to define the cell orientation
  79. What are the four general steps involved in repair by connective tissue or fibrosis?
    • �Angiogenesis- Formation of new blood vessels at the site of injury (neovascularization)
    • �Migration and proliferation of finroblass to the site of injury
    • �Deposition of ECM by the fibroblasts
    • �Maturation and remodeling of the fibrosis tissues by macrophages
  80. What are the six steps of neovascularization?
    • �Dilation and increased permeability of the preexisting blood vessel at the site of angiogenesis
    • �Proteolysis of ECM to break down the basement membrane
    • �Migration of endothelial cells toward a chemoattractant angiogenic stimulus a the site of injury
    • �Endothelial cell proliferation just behind the leading edge of migrating cells
    • �Once enough cells are present proliferation stops, lumen formation occurs and the endothelial cells self organize into tubes
    • �Recruitment and organization of accessory cells to complete the mature vessel
  81. what molecules regulate neovascularization?
    Fibroblast growth factors, vascular endothelial growth factor
  82. What are the two steps in scar formation?
    • �Emigration and proliferation of fibroblasts at site of injury
    • �Deposition of ECM components by fibroblast at site of injury
  83. What factors regulate scar formation?
    PDGF, FGF, TGF beta
  84. What are the six overall steps in cutaneous wound healing?
    • �Induction of acute inflammatory response by injury
    • �Parenchymal cell regeneration
    • �Migration and proliferation of parencymal (epithelial) and connective tissue cells
    • �Synthesis of ECM proteins
    • �Remodeling of parenchymal elements to restore tissue function
    • �Remodeling of connective tissue to restore wound strength
  85. What are the steps to healing by first intention?
    • �Incision fills with clotted blood which forms a fibrin clot and scab
    • �Neutrophils migrate to clotted blood
    • oThey produce factors the stimulate epithelial cell proliferation at the wound
    • oEpithelial cells advance towards eachother and secrete basement membrane componants to pinch of the clot
    • oEpithelial cells meet beneath a surface of scab and form a thin layer of epithelium
    • �Macrophages replace neutrophils in stromal (subcutaneous) space
    • oResolve inner scab and produce factors that promote neovascularization, fibroblast migration, and ECM deposition which leads to restoration of interstitial volume
    • �Epithelium (epidermal cells) proliferate and epidermis recovers its normal thickness. Surface scab falls off.
    • �Inner scab is resolved and replaced by a fibrous union. Inflammatory processes are resolved.