Cell Injury

  1. List 5 biochemical themes in cell injury
    ATP depletion, generation of ROS, loss of Ca homeostasis, altered plasma membrane permeability, mitochondrial damage
  2. Hypoxia causes what type of morphogenic change? Why?
    Hypoxia impairs oxidative phosph. leading to decreased ATP. Lack of ATP causes a disruption in homeostasis and a net gain of solute causing the cell to swell.
  3. Isoosmotic gain of water has what effect on organelles?
    mitochondrial swelling, dilation of the ER causing decreased protein synthesis and increased lipid deposition
  4. How does hypoxia effect cellular metabolism?
    decreased ox. phosph. and increased glycolysis. increased glycolysis decreases intracellular pH leading to chromatin clumping
  5. what effect does hypoglycemia produce on cells?
    lack of ATP production bc no substrate to use for energy (loss of homeostasis)
  6. list 3 types of ROS
    Superoxide (O2), Hydrogen peroxide, hydroxyl radicals
  7. how is superoxide inactivated?
    superoxide is inactivated by superoxide dismutase to form hydrogen peroxide
  8. how is hydrogen peroxide metabolized?
    detoxified by glutathione peroxidase and catalase
  9. how are hydroxl radicals generated?
    by hydrolysis of water by ionizing radiation or by transitional metals Fe or Cu
  10. how do ROS damage cells?
    lipid peroxidation, protein cross-linking, thymidine and guanine single strand DNA breaks
  11. what intracellular antioxidant systems exist?
    Superoxide dismutase (O2), catalase (H2O2), glutathione peroxidase (H2O2)
  12. what extracellular antioxidant systems exist?
    vitamins A, C, E
  13. what type of cell injury occurs by increased cytoplasmic Ca?
    high Ca levels will activate various degradative enzymes
  14. list 4 degradative enzymes activated by high Ca levels
    phospholipases, proteases, endonucleases, ATPase
  15. list 3 outcomes of cellular injury
    reversible cell injury, adaptation, cell death
  16. what is the single biochemical event influencing cell death
    there is no single biochemical event that equates with cell death
  17. what morphologic changes occur during necrosis?
    cell swelling, protein denaturation, organelle breakdown, inflammation, nuclei changes (karyolysis, pyknosis, karyorrhexis, or total loss)
  18. Describe Coagulative Necrosis
    most common form of necrosis, cytoplasmic proteins are coagulated, nucleus is lost
  19. Describe Liquefactive necrosis
    has lots of pus (purulence) and the tissue is totally digested by release of lysosomal enzymes during acute inflammatory response
  20. describe caseous necrosis
    associated with M. tuberculosis infection. loss of tissue architecture and amorphous pink granular material
  21. describe fat necrosis
    dead adipocytes give a "soap bubble" histological appearance, common in breast trauma or pancreatitis
  22. describe 4 morphologic features of apoptosis
    cell shrinkage, chromatin condensation/fragmentation, apoptotic bodies formation, phagocytosis without inflammatory response
  23. what are 5 ways a cell can be signaled to start apoptosis
    intrinsic, Fas Ligand-receptor binding, removal of trophic signals, ROS/radiation/toxins, cytotoxic T cells
  24. what is the function of the Bcl-2 gene family?
    regulation of permeability of the mitochondrial membrane
  25. how do the Bcl-2 and Bcl-x genes affect apoptosis?
  26. how do the bax and bak genes affect apoptosis?
  27. what effect does cytochrome-c have?
    it is released from outer mt membrane and disrupts inhibitory function of Bcl-2, in other words it stimulates apoptosis
  28. what effect do caspases have on the cell? what substrates does it have?
    apoptosis, substrates include cytoskeletal and nuclear matrix proteins, DNase and transcription proteins
  29. what are the differences between apoptosis and necrosis in terms of stimuli?
    apoptosis: physiologic and pathologic; necrosis: hypoxia and toxins
  30. what are the differences between apoptosis and necrosis in terms of cellular morphology
    apoptosis: single cells, shrinkage; necrosis: multiple cells, swelling
  31. what are the differences between apoptosis and necrosis in terms of ATP
    apoptosis: ATP dependent; necrosis: ATP independent
  32. list 4 cellular adaptations
    cell size (atrophy vs hypertrophy), cell number (hyperplasia), cell differentiation (metaplasia), intracellular accumulations
  33. what are two etiologies of hypertrophy?
    response to trophic signals, response to increased functional demand
  34. list 2 examples of abnormal hormone stimulation
    anabolic steroids: hypertrophy; overproduction of TSH due to iodine deficiency and induces thyroid follicle hypertrophy (goiter)
  35. define barrett's esophagitis and explain what type of cellular adaptation it displays
    normal stratified squamous epithelium of esophagus replaced due to prolonged exposure to gastric reflux---metaplasia
  36. list 4 mechanisms of intracellular accumulations
    abnormal metabolism, lack of an enzyme, abnormal protein folding/transport, ingestion of indigestibile material
  37. define steatosis
    fatty liver; abnormal accumulation of triglycerides within parenchymal cells of the liver, heart, kidney and skeletal muscle
  38. list 6 etiologies of steatosis
    obesity, diabetes, alcohol, anorexia, toxins, protein malnutrition
  39. xanthoma is a result from what?
    cholesterol accumulation
  40. atheromas of atherosclerosis in vessels are caused by what?
    cholesterol accumulation in macrophages
  41. list 3 results from abnormal protein accumulation
    a1-anti-trypsin deficiency (impaired folding), mallory bodies (impaired secretion), neurofibrillary tangles in Alzheimer's (accumulation of microtubule-associated proteins)
  42. what is Lipofuscin
    endogenous brown-yellow pigment, lipoprotein complex due to ROS peroxidation of membranes
  43. what is hemosiderin
    yellow-brown pigment due to aggregates of ferritin micelles from excess iron. can lead to hemosiderosis
  44. define hemochromatosis
    genetic disease associated with cell death due to uncompensated hemosiderin accumulation
  45. what is bilirubin
    end product of heme metabolism that accumulates in hepatocytes and bile ducts due to hemolysis, obstructed bile flow and/or hepatocellular disease
Card Set
Cell Injury
Covers cell injury, cell death and cell adaptations