pathology exam1

  1. Pathology
    study of funcitonal and structural changes in cells, tissues and organs that underlie disease
  2. four core aspects of pathology
    • etiology=cause
    • pathogenesis=mechanisms of development
    • morphological changes=structural alterations of cells and organs
    • clinical significance=functional causes of morphological changes
  3. name four types of cell adaptation
    • hyperplasia
    • hypertrophy
    • atrophy
    • metaplasia
  4. when does cell adaptation occur?
    response to increased demand, decreased demand, or chronic irritation
  5. hyperplasia
    increased NUMBER of cells

    occurs if cells have ability to replicate i.e. mucosa of gastrointestinal tract
  6. hypertrophy
    increased SIZE of cells

    less regenerative capacity, so get bigger instead of replicating, i.e. heart muscle
  7. do uterine cells undergo hypertrophy or hyperplasia to meet the demands of pregnancy?
  8. atrophy
    diminuation in size
  9. Some reasons cells atrophy (7)
    • decreased workload
    • loss of innervation
    • diminished blood supply
    • inadequate nutrition
    • loss of endocrine stimulation
    • aging
    • pressure
  10. metaplasia
    one adult cell types is replaced by another

    usually occurs in epithelial tissue as a result of chronic irritation
  11. reversible cell injury
    cell has potential to return to function of harmful stimulus is withdrawn
  12. irreversible cell injury
    leads to cell death by necrosis or apoptosis
  13. stimuli that cause cell injury (6)
    • oxygen deprivation
    • physical agents
    • chemical agents
    • infection agents
    • genetic derangements
    • nutritional imbalances
  14. hypoxia
    insufficient oxygen in blood stream
  15. ischemia
    insufficient blood supply
  16. Why is ischemia often more damaging to cells than hypoxia?
    B/c not only is there too little oxygen, but there is also too little nutrients and no removal of wastes
  17. examples of physical agents (5)
    • mechanical injury
    • temperature
    • barometric pressure
    • radiation
    • electric shock
  18. example of problem with protein production
    alpha-thalassemmia where one hemoglobin molecule is not produced and the oxygen carrying capacity of the blood is compromised
  19. example of protein function that cause cell injury
    sickle cell anemia where hemoglobin molecules are structurally unstable
  20. Tay-Sachs
    enzyme needed for removal of waste products is missing
  21. Name 5 essential strutures or functions of the cell
    • 1. generation of ATP by mitochondria
    • 2. Integrity of mitochondria
    • 3. Transmembrane calcium homeostasis
    • 4. Protection against oxidative stress
    • 5. Membrane impermeability
  22. What happens when ATP production is reduced by just 5-10%?
    • -Na+/K+ pump compromised
    • -switch to anaerobic metabolism -->Accumulation of "H+ so lower pH
    • -influx of Ca++ from extracellular space
    • -dissolution of protein synthesis apparatus
  23. What happens when there is damage to electron transport chain resulting in less ATP?
    proton motive force of inner mitochondrial membrane disrupted

    Cytochorme c leaks out fo inner mitochondrial membrane, promoting apoptosis
  24. What happens with calcium when there is cell injury?
    More calcium enters permeable membranes of cell. Increase in cytosolic calcium activates enzymes that cuases cells to eat themselves inside out.
  25. free radical
    molecule with an unpaired electron in its outer orbit

    e.g. hydroxl (OH), hydrogen pyroxide (H2O2), superoxide anion (O2-) nitric oxide (NO)
  26. What can happen when free radicals react with other molecules?
    • lipid peroxidation (disruption)
    • denatured proteins
    • breaks in DNA

    free radicals produce more free radicals, increasing oxidative stress of cell
  27. antioxidant
    scavenge free radicals
  28. Two changes that characterize irreversible injury include
    mitochondrial function cannot be restored

    membrane integrity cannot be restored
  29. list morphological features of cell injury (4)
    • mitocondrial swelling
    • alterations of plasma membrane
    • dilaion of the ER, with dissociation of ribosomes
    • nuclear changes
  30. if cell injury persists beyond a few hours
    cellular swelling due to loss of ability to maintain electrolyte balance

    hydropic change = vacuolar degeneration - ER swollen
  31. two morphological patterns of cell death
    necrosis = cell death due to secondary, exogenous injury

    apoptosis = programmed cell death
  32. What happens with necrosis?
    tissue distruction by endogenous enzymes from either leaky lysosomes or inflammatory cells

  33. types of necrosis (4)
    • 1. coagulative (ischmic injury)outline of cells remain but intracellular detail lost "mummified"
    • 2. liquefactive inflammatory cells digest tissue creating pus made of cellular debris. Common in bacterial and fungal infections
    • 3. caseous found inside a granuloma (inflammatory response to certain fungi or mycobacteria) contains pus adn organism. Thick, white and cheesy.
    • 4. Fat - death fo fat cells. Can be coagulative r liquefactive
  34. dystrophic calcification
    formation of calcium crystals in areas of necrosis

    calcium binds with phospholipids present in fragments of degenerated or dying cells.

    typical in atheroschlerosis and pancreatitis
  35. apoptosis
    Programmed cell death - cell in induced to dismantle itself

    Plasma membrane stay intact so there is no destruction of surrounding tissue or initiation of inflammatory response
  36. How are apoptopic cells cleared from system
    phagocytes recognize symbols on cell membranes
  37. What is the most powerful stimulus for apoptosis?
    irreparable damage to DNA by radiation or chemo
  38. stimuli that can cause apoptosis
    • viral disease
    • oxidative damage
    • heat
    • hypoxia
    • cytotoxic T lymphosite
  39. end result of apoptosis
    production of caspases, enzymes that digest the cytoskeleton and activate enzymes that digest the intracellular contents

    plasma membrane creates pockets of cellular contents which are engulfed by phagocytes

    plasma membrane NOT broken down so no inflammatory response
  40. common cellular accumulations
    • lipofuscin - lipid accumulation due to free radical injury
    • hemosiderin - iron in cell cytoplasm
    • protein - chronic diseases of the kidney can cause accumulation in proximal tubules
    • fat-in hepatocytes due to impairment of liver cells to metabolize fatty acids
  41. areas of inflammation and needle shaped clear spaces are ...
    the footprint of cholesterol derived from cell membranes during necrosis
Card Set
pathology exam1