Path L1 Cell adaptation.txt

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kepling
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98913
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Path L1 Cell adaptation.txt
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2011-09-09 00:15:13
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Path L1 Cell adaptation
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Path L1 Cell adaptation
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  1. What is the main cause of adaptation?
    Stress
  2. What is hypertrophy?
    increase in cell size and organ size
  3. What is hyperplasia?
    increase in cell # and organ volume
  4. What types of tissues can become hypertrophic?
    Heart & Skeletal mm
  5. What types of tissues are affected by hyperplasia?
    glands and ducts
  6. What is atrophy?
    reduced size of organ due to reduced cell size and reduced number
  7. What is metaplasia?
    transformation that is reversible and occurs in adult cell types
  8. T/F Metaplasia is cancerous?
    F, dysplasia can lead to cancer
  9. What are two indications of a reversible change?
    • Fatty change
    • swelling
  10. What type of disease of the heart is irreversible?
    MI
  11. hypertrophy: Pressure overload vs. Volume overload?
    • Pressure overload: Concentric
    • Volume overload: Eccentric
  12. What are the two stimuli for hypertrophy?
    Pressure and volume overload
  13. Three mechanisms of cardiocyte hypertrophy? (MAG)
    • Mechanical stretch
    • agonists (Beta)
    • growth factors
  14. How do cardiocytes go through hypertrophy?
    • More actin and myosin due to growth factors
    • micro RNAs
  15. How do nuclei appear in a hypertrophic cardiocyte?
    • hyperchromatic
    • boxy, large
  16. How do fat cells grow differently pre- and post-puberty?
    • Pre: increase in number
    • Post: hypertrophy/atrophy
  17. What causes subcellular hypertrophy of the SER?
    hyperactive cytochrome P450 system due to excessive alcohol/drug use
  18. How does a person react to drugs with a hypertrophied SER?
    • adapt
    • tolerance
  19. What common class of drugs can induce SER Hypertrophy?
    Barbituates
  20. If a person is taking barbituates for convulsion and starts to drink, what will be the result?
    Less effectivity and uptake of barbituates b/c it shares the system with alcohol
  21. What is the physiological response for the myometrium of the uterus to hormones?
    Hypertrophy
  22. What adaptation occurs in breasts?
    Hyperplasia
  23. What causes hyperplasia of breasts?
    hormones
  24. What types of cells adapt via hyperplasia?
    Labile: epithelial and bone marrow cells
  25. What organ adapts via compensatory (regeneration) hyperplasia?
    Liver via GFs
  26. How does the endometrium of the uterus adapt?
    Hyperplasia, estrogen
  27. How does the prostate gland adapt?
    Hyperplasia, DHT
  28. What stimulates erythroid hyperplasia (aka erythropoietin)?
    hypoxia
  29. What is polycythemia?
    increased RBC count
  30. What hormone causes Adrenal and thyroid gland hyperplasia?
    • Adrenal: ACTH
    • Thyroid: TSH
  31. What are four GF mediated pathologic hyperplasia examples and their causes?
    • 1) Keloid scar: fibroblasts
    • 2) Hypertrophic scar: Myofibroblasts
    • 3) Viral warts: HPV
    • 4) Psoriasis: cytokines, epidermal squamous cells
  32. Where are the two places in the human body where cancer and hyperplasia can exist?
    • Breast
    • Endometrium
  33. What is the most common form of Atrophy?
    Disuse atrophy
  34. T/F cells cannot recover from atrophy?
    F, they can recover
  35. What are the two methods of cell loss during atrophy?
    • Autophagy
    • Apoptosis
  36. What areas of the body are affected by endocrine atrophy?
    • Breast
    • Endometrium of uterus
    • vaginal epithelium
    • Adrenal cortex (lack of ACTH)
  37. What is a sign of denervation atrophy?
    grouped atrophy of mm
  38. What type of atrophy is caused by Charcot marie tooth syndrome?
    Denervation atrophy
  39. What type of atrophy is a hereditary loss of motor neurons?
    SMA: Spinal muscle atrophy (Werdnig-Hoffman)
  40. What atrophy is caused by Polio? what is destroyed?
    • Denervation atrophy
    • Anterior horn cells destroyed
  41. T/F bilateral atrophy is caused by a hormone change?
    T
  42. What type of atrophy does atherosclerosis cause?
    Blood loss atrophy
  43. T/F Blood loss atrophy is unilateral?
    T (but can be bilateral if full occlusion)
  44. What are two causes of blood loss atrophy?
    • 1) Pressure: tumor, twisting of testes, etc...
    • 2) diminished blood supply: injury, atherosclerosis, ischemia
  45. What type of atrophy are Marasmus and Cachexia? Causes?
    • Inadequate Nutrition Atrophy
    • Marasmus: autophagy from protein malnutrition
    • Cachexia: TNF alpha, inflammation, cancer
  46. What are the two mechanisms of Atrophy?
    • 1) ubiquitin-proteosome path (high in infection of HIV, TB and cancer)
    • 2) Autophagy: digest cytoplasmic organelles in lysosomes
  47. What are two remnants of autophagy?
    • 1) residual bodies
    • 2) Lipofuscin pigment
  48. What are the 2 causes of Metaplasia?
    • Stress
    • irritation
  49. If a muscle is injured, what type of metaplasia will occur?
    • Myositis ossificans: fibroblasts will form bone b/c mm can't regenerate
    • ** AKA Osseus metaplasia
  50. What is the most common metaplasia?
    Fat metaplasia
  51. Within cells, what is the most common metaplasia?
    Squamous metaplasia (from glandular or columnar cells)
  52. What is columnar (glandular) metaplasia?
    Squamous cells replaced by columnar cells
  53. What organ is affected by columnar metaplasia? Why?
    • Esophagus, acid reflux
    • * Barrett's esophagus
  54. Why does glandular metaplasia occur?
    To help produce more mucous in the air and food tracts of the body
  55. What are the three pathways of cell death?
    • Necrosis: Pathologic
    • Apoptosis: Path and physiologic
    • Autophagy
  56. What are the characteristics of the three styles of cell death?
    • 1) Necrosis: lipases, proteases and lysosome material released to rupture cell
    • 2) Autophagy: Lysosome degradation
    • 3) Apoptosis: cellular blebbing due to shrinkage
  57. What regulates autophagy?
    Autophage genes, ATGs
  58. what cell injury occurs when ATP is depleted and oxidative phosphorylation is decreased?
    reversible cell injury
  59. What cellular changes occur during a reversible cell injury?
    • 1) swelling
    • 2) fatty vacuoles appear (steatosis)
  60. What happens to mitochondria during reversible cellular injury?
    Mitochondrial densities
  61. what color does a cell going through reversible cell injury appear? Why?
    • Pink
    • Due to polysomes being released into cytoplasm and eiosinophilic dye
  62. when is cellular injury irreversible? (3 reasons)
    • 1) mitochondrial dysfunction
    • 2) membrane lost
    • 3) nuclear dissolution
  63. What occurs at the end of an irreversible cellular injury?
    Necrosis
  64. What are two methods of necrosis?
    • 1) Autolysis
    • 2) lysosomal enzymes from leukocytes from inflammation
  65. What are the three nuclear morphologies of Necrosis?
    • 1) Karyolysis: fading of nucleus
    • 2) Nuclear pyknosis: shrinking of nucleus
    • 3) Karyorrhexis: destruction of pyknotic nucleus
  66. Name the six types of Necrosis?
    • 1) Gangrenous: wet and dry
    • 2) Coagulative: membranes present
    • 3) Caseous: cottage cheese
    • 4) Fatty:
    • 5) Fibrinoid:
    • 6) Liquefactive: lipases degrading, no membranes
  67. What kind of necrosis is acute tubular necrosis of kidney? What is present?
    Coagulative (cell membranes still present)
  68. What type of necrosis is commin in MI?
    Coagulative necrosis due to occlusion
  69. An infarction will always lead to what type of necrosis?
    Coagulative necrosis
  70. What cells clear coagulative necrosis?
    Phagocytes?
  71. When does Liquefactive necrosis occur?
    • Stroky/CNS hypoxia
    • Abscesses from infection
  72. What degrades liquefactive necrosis?
    Inflammatory cells
  73. What necrosis occurs in the brain? Why?
    • Liquefactive
    • This occurs b/c coagulation cannot stay around due to lack of fibroblasts
  74. What causes gangrenous necrosis?
    infection and ischemia
  75. Diff b/t dry and wet gangrenous necrosis?
    • Dry: ischemia predominates
    • Wet: ischemia and infection together
  76. three common signs of caseous necrosis?
    • Cavitates
    • TB
    • macrophage granulomas
  77. Two types of Fat Necrosis?
    • Traumatic: injury or surgery to fatty tissue
    • Enzymatic: Lipases released from pancreas
  78. Common organ affected by Fat Necrosis?
    Breasts
  79. What is Fibrinoid Necrosis?
    Immune mediated blood vessel damage, Eiosinophils in cell walls
  80. What causes ATP to deplete?
    Hypoxia
  81. Four cellular problems when ATP depletes?
    • 1) Na enters cell = K leaves = water enters = swelling
    • 2) Glycolosis = increase in lactic acid = decrease pH
    • 3) loss or ribosomes = lack of proteins = lack of APO for shipping fat = fat buildup in cell
    • 4) Protein folding abnormal
  82. Which occurs faster, ischemia or hypoxia?
    Ischemia
  83. What is the main cause of hypoxia?
    Shock due to decreased systemic perfusion
  84. Two main problems of full ischemia?
    • ATP depletion = swelling
    • CK/Troponin released into body
  85. five common causes of mitochondrial damage
    • Hypoxia
    • Drugs/Toxins
    • increased cellular calcium
    • oxidative stress
    • genetic disposition
  86. After mitochondrial damage, what causes Necrosis and Apoptosis?
    • Necrosis: lack of ATP production
    • Apoptosis: cytochrome C released from pores
  87. How does calcium increase occur in cells?
    • Release of sequestered calcium
    • influx b/c of pores that are not functioning
  88. What molecules disrupt plasma membranes making them permeable to Calcium?
    • Phopholipase A2
    • Proteases
  89. What metabolic system can increase free radicals?
    oxidation/reduction of oxygen in peroxisomes

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