Cell Injury

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Author:
Aleksbaron
ID:
260897
Filename:
Cell Injury
Updated:
2014-02-09 10:39:08
Tags:
OBMP 8004
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Description:
Exam 1
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  1. Steady state of a cell is called?
    Homeostatis
  2. Acute and transient cell damage leads to
    reversible cellular swelling, fatty change
  3. Progressive and severe damage will lead to
    irreversible damage like necrosis or apoptosis
  4. Hyperplasia or hypertrophy
    inc demand or inc stimulation
  5. Atrophy?
    dec nutrients or decreased stimulation
  6. Chronic irritation (physical or chemical) leads to?
    Metaplasia
  7. Adaptation can be divided into?
    PHysiologic: hormone induced hypertrophy of breast and uterus during pregnancy.

    Pathologic: response to stress to escape injury
  8. Increase in cell size
    Hypertrophy
  9. Increase in cell number
    Hyperplasia

    Example: Benign prostatic hyperplasia
  10. Pathologic hypertrophy example?
    HTN or aortic stenosis results in stretching of the cardiac muscle (mechanical or trophic triggers)
  11. Pathologic hyperplasia example?
    Hyperplasia of fibroplasts in response to a wound stress (growth factors)

    Acanthosis nigricans: excess epidermal growth factor production of malignant tumor
  12. Gingival hyperplasia causes?
    Dilantin, Cyclosporine

    Epulis fissuratum, Parulis (sinus tract), pulpal hyerplasia, hypekeratosis (linea alba)
  13. Hyperplasia of some tissues can lead to malignant neoplasia, example?
    Endometrium
  14. Define atrophy?
    shrinkage in size of the cell by loss of cell substance, dec protein synthesis, inc protein degradation
  15. Define metaplasia?
    Reversible change from one adult cell type (epithelial or mesenchymal) to another

    reprogrammed to differentiate along a new path
  16. List some causes of atrophy?
    • 1. aging
    • 2. dec workload
    • 3. loss of innervation
    • 4. dec blood supply
    • 5. dec nutrition
    • 6. dec endocrine stimulation
  17. What is autophagy?
    in time of nutrient deprivation, proteins are degraded by lysosomes after being packaged into autophagosomes.
  18. What two cellular changes can be premalignant in some tissues?
    Metaplasia and Dysplasia
  19. What are some mechanisms leading to intracellular accumulations?
    • 1. Abnormal metabolism (fatty liver cells)
    • 2. Lack of enzyme
    • 3. Defective protein folding, transport
    • 4. Uptake of indigestible material
  20. Another name for fatty change in liver?
    Steatosis
  21. Dystrophic calcification?
    deposition of calcium at sites of injury
  22. Metastatic calcification?
    deposition of calcium in normal tissues (hypercalcemia, high PTH)
  23. Telomere shortening leads to ?
    Replicative senescene
  24. What are some principle mechanism of cellular injury?
    • 1. ROS
    • 2. dec ATP
    • 3. Mitochondrial damage
    • 4. Membrane damage
    • 5. Protein misfolding
    • 6. Entry or Calcium
  25. Cell injuries leading to necrosis?
    Ischemia or hypoxia: ischemia faster damage

    Ischemia and reperfusion: inflammatory cells add insult

    Chemical
  26. Difference in cell size from necrosis to apoptosis?
    • N: Enlarged
    • A: reduced
  27. Difference in nucleus in necrosis vs. apoptosis?
    • N: pyknosis, karyorrhexis (nuclear fading), karyolysis
    • A: fragmentation into nucelosome-size fragments
  28. Difference in plasma membrane necrosis vs. apoptosis?
    • N: disrupted
    • A: Intact, but reorganized
  29. Difference in cellular contents necrosis vs. apoptosis?
    • N: Enzymatic digestion, leakage
    • A: Intact; may be released in apopotic bodies
  30. Difference in inflammation necrosis vs. apoptosis?
    • N: Frequent
    • A: none
  31. Necrosis is always from pathology (irreversible cell injury)
  32. Apoptosis can be pathologic (DNA damage) or physiologic (unwanted cells)
  33. Consequence of chronic inflammation or inflammatory exudate?
    Fibrosis and scarring, deposition of fibrous connective tissue in place of original cells

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