Cell Pathology

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Cell Pathology
2011-02-19 15:58:02
cell cancer injury

Chpt 1
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  1. Cells
    smallest functional unti that an organism can be divided into and return necessary charateristic for life functions.
  2. Tissues
    Larger funtional unit of cells that are grouped together due to their funtion.
  3. Eukaryotic Cells
    Plasma membrane, nucleus, and cytoplasm.
  4. Plasma Membrane
    It is a cell membrane that is made up of phospolipids, proteins, and cholesterol. It participates in the generation and conduction of the electrical currents like in nerve and muscle. Also it's semipermeable and seperates environment both intracellular and extracellular.
  5. Nucleus
    It can be round or elongated structure. Has a nuclear envelope that has an inner membrane and a outer membrane
  6. Cytoplasm
    contains mostly water. Contains cytoskeleton as well as organelles and fluid (cytocell). Embedded in the cytoplasm which function as organs of the cell are the E.R., golgi aparatus, lysosomes, perioxisomes, proteasesomes, and mitochondria.
  7. Endoplasmic Reticulum
    Primary site of protein synthesis. Rough E.R- contains ribosome whic can synthesize proteins. Smooth E.R- no ribosomes, no protein synthesis, but synthesis of lipid molecules, steroid hormones, and lipoprotein. Mteabolizes and detoxifies drugs.
  8. Golgi Aparatus
    Modify substances transported to them into secretory granules or vesicles. Carbohydrate synthesis.
  9. Lysosomes
    Gigestive organelles of the cell. Breakdown and digest worn out cell parts or foreign bacteria. Lysosomal enzymes are synthesized in the Rough E.R. and transported to the Golgi aparatus where they're chemically modified and packaged for transport.
  10. Perioxisomes
    Degrades peroxides. Breaks down very long chain fatty acids that mitochondrial enzymes can't. In liver, these aid in formation of bile acids Proteasomes.
  11. Mitochondria
    power plant of the cell. Transform compounds into enerygy. Contain enzymes needed for capturing most of the energy in food and converts it into energy.
  12. Cytoskelton
    Controls the shape and the movement of the cell. Contains microtubules- slender, stiff tubular structures that influence shape. effect the movement of the cilia and of chromosomes during cell division. Contains microfilaments- present in muscle cells. Function or supporting and maintaining the shape of cells.
  13. Mechanism of disease as related to cell injury, aging, and death
    • change in response to stress- change in cell size, in cell number, in cell type.
    • may lead to: atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia.
  14. Atrohpy
    Lower and more effecient level of functioning. Decrease O2 consumption and other functions.
  15. General causes of Atrophy
    Disuse, denervation, loss of endocrine stimulation, inadequate nutrition, and ischemia or decreased bL. flow.
  16. Hypertrophy
    Increase in cell size w/ amt of functioning tissue mass. Result from increase workload of organ or body part. Increases O2 demand, ATP use.
  17. Hyperplasia
    • Increase number of cells in tissue orin organ. Occurs as a response to an appropriate stimulus and ceases once the stimulus has been removed. Physiologic- hormonal and compensatory.
    • Non physiologic- due to excessive hormone stimulation or the effect of growth factors on target tissues.
  18. Metaplasia
    Reversible change in which one cell type is replaced by another adult cell type. Usually from chronic irritation and inflammation and allows for substitution of cells that are better able to survive.
  19. Dysplasia
    Derranged cell growth of a specific tissue that results ub cells that vary in size, shape, and organization. Can be chronic irritation and inflammation. Implicated as precursor to cancer but doesn't necessarily lead to cancer.
  20. Intracellular Accumulation
    Build up of substances thats cells can't immediately use or eliminate. Accumulate in the cytoplasm, organelles like lysosomes or nucleus. Genetic disorders that disrupt enzymatic degration.
  21. Pathologic Calcification
    Abnormal deposits of calcium salts, iron, magnesium, and other minerals.
  22. Dystrophic Calcification
    Dead and dying tissue atheroscerosis cause of organ disfunction.
  23. Metastatic Calcification
    Occur in normal tissue, increase serum calcium levels. happens in lungs, kidneys, and bl. vessels. Certain cancer, pagets disease, and vit. D intoxication.
  24. Cell Injury and Death
    Injury from physical agent, radiation injury, chemical injury, injury from biologic agents, and injury from nutritional imbalances
  25. Injury from physical agents
    • mechanical forces- split or year tissues, fx bones, injured bl. vessels, and disrupt bl. flow
    • Extreme temperatures- heat- vascular injury increases cell metabolism, disrupting cell membrane, and coagulation of bl. vessels.
    • cold- increases blood viscosity, vasoconstriction, and capilary stasis.
  26. Radiation injury
    • Ionizing radiation- used in tx of cancer. clincal manifestation results from acute cell injury.
    • UV radiation- increasing energectic rays that are powerful enough to disrupt intracellular bonds.Damages DNA.
    • Nonionizing radiation- causes vibration& rotation of atoms and molecules eventually creating thermal energy. Rarely associated w/ skin burns. Infared light, ultrasound, microwaves, and laser energy.
  27. Chemical injury
    injures cell membrane and other cell structures, block enzymatic pathways, coagulate cell proteins, disrupt osmotic & ionic balance of cells. ex- drugs, lead, and mercury toxicity.
  28. Injured from biologic agents
    able to replicate and can continue to prduce their injurious effects. virus to bacteria. viruses can enter into the call and become incorporated into its DNA and AIDs.
  29. Injury from nutritional imbalance
    nutritional excesses and defficiences predispose cells to injury-obesity. Can occur from deficiences like iron,scurvy, ricketts.
  30. Mechanism of Cell injury
    • Free radical injury- damage cell which cause unstable & highly reactive molecular bonds.
    • Hypoxic cell injury- deprives the cell O2 & interupts oxidative metabolism & generation of ATP.
    • Impaired calcium homeostasis- can affect smooth muscle contraction and glycogen breakdown.
  31. Reversible cell injury and cell death
    impairs cell funtion but doesn't result in death. causes cellular swelling>result of hypoxic cell injury. Fatty change- intracellular accumulation- fat metabolism is impaired during cell injury & fat accumalates in the cell.
  32. Programmed cell death
    balance of cell proliferation and cell death. apoptosis- removes injured or worn out cells and control tissue regeneration. Thought to be responsible for several normal physiologic processes.
  33. Necrosis
    Cell death in an organ or tissue that's still part of a living person. Unregulated enzymatic digestion cell components, loss of cell membrane integrity w/ uncontrolled release of products of cell death into intracellular sppace & initiation of inplammatory response.
  34. Gangrene
    considerable mass of tissue that undergoes necrosis. ex- dry, moist, or gas.
  35. Cell aging
    cell functions decline w/ age- unsure of why.
  36. Replicative senescence
    - limited capacity for replication DNA mutation over time.
  37. Genetic influences
    gene may determine longevity
  38. Accumulation of environmental and genetic damage
    damage eventually accumulates to a level suffiecient to result in the physiologic decline associated w/ aging
  39. Syndromes of Premature Aging
    increase age of onset of aging and increases rates of progression.
  40. Benign
    • character that doesn't threaten health or life.
    • slow, progressive rate of growth.
    • benign neoplasms are well differentiated tumors that resemble the tissue of origin but have lost the ability to control cell proliferation, grow by expansion.
  41. Malignant
    • Tending or threatening to produce death, harmful.
    • Malignant neoplasms less well differentiated tumors that have lost the ability to control both cell proliferation & differentiation.
    • Growth is disorganized and uncontrolled.
    • Cell may break loose and travel to different sites to form metastases.
  42. Causes of Cancer
    • Genetic and molecular- mechanism that characterize the transformation of normal cells into cancer cells.
    • External & more contexual factors- age, heredity, and environmental agents that contribute to its development and progression
  43. Genetic & molecular basis of cancer
    • Cancer associated genes:
    • Proto oncogenes, loss of tumor, and MicroRNA genes.
  44. Proto-onocgenes
    overactive genes that become cancer causing if mutated- point of mutation, chromosomal translocation, and gene amplification
  45. Loss of Tomor
    • supressor genes- underactive; normal cells have regulatory genetic mechanism that protect them against activated or newly acquired oncogenes.
    • tumor supressor has become inactivated which causes unregulated growth to begin.
  46. MicroRNA genes
    single RNA strand that regulates gene expression that can undergo rearrangements, deletions, amplifications: can be tumor supressor or oncogenes depending on how its paired.
  47. Epigenetic Mechanism
    • involve changes in the patterns of gene expression w/o a change in DNA.
    • May silence tumor supressor gene which will still be present but not expressed.
  48. Molecular Cellular Pathway
    • Defect in DNA repair mechanism caused by chemical, radiation, viruses or inherited.
    • Disorders in growth factor signaling pathways which eventually may cause unregulated cell growth & proliferation.
  49. Tumor cell transformation
    • 3 steps:
    • Initiation- exposure of cells to carcinogenic agents.
    • promotion- induction of unregulated accelerated growth in already initiated cells by various chemicals and gorwth factor.
    • Progression- tumor cells acquire malignant phenotype changes that promote invsiveness, metastatic competence, autnomous growth tendecies, and increased karyotypic instability
  50. Host and environmental factors
    heredity, hormones, obesity, immunologic, chemical agents, radiation, viral and microbial agents.
  51. Grading of cancer
    • used to determine the course of disease and aid in selecting appropriated treatment or management plan.
    • Microscopic exam of cancer cells to deteremine level of differentaion and # of mitosis.
    • Grade scale- I- well differentiation IV- poorly differentiated and display marked anaplasia.
  52. Staging of cancer
    • used to determine the course of disease and aid in selecting appropriate treatment or management plan.
    • Helps to estimate prognosis. Size of primary tumor, it extent of local growth, lymph node involvement, and presence of distant metastasis.
  53. Surgical Treatment
    • according to grade, stage, and location.
    • determined of the extent of disease.
    • tumor growth rate and invasiveness.
    • if tumor is too small and has well defined margins often the entire tumor can be removed.
    • if mor extensive, it will be morew difficult if not impossible to remove.