Path 1 Block 1

  1. Etiology
  2. Pathogenesis
    Mechanism of development:
  3. Morphologic Changes
    Structural changes induced in the cells and organs of the body
  4. Clinical Significance
    Functional consequences of the morphological changes
  5. Gross/Histologic
  6. Prognosis
    Expected outcome
  7. Necropsy
    study of cadavers
  8. Surgical Pathology
    examination of tissues from living patients
  9. Cytopathology
    study of individual cells
  10. Clinical Pathology
    analysis of various specimens
  11. Forensic Pathology
    medicolegal investigation into death
  12. Closed Biopsy
    needle inserted into mass to obtain a bit of tissue
  13. Open Biopsy
    incision made to obtain a larger mass of tissue
  14. Excisional Biopsy
    mass or entire organ removed
  15. FNAC
    • fine needle aspiration cytology
    • - thin bore needle used to obtain a few cells
  16. Frozen Sections
    done to get a rapid diagnosis while the patient is on the operating table
  17. Routine stains - Hematoxylin/Eosin
    • hematoxylin - nuclei
    • eosin - cytoplasm
  18. Mucicarmine Stain
  19. Fontanna-Mason Stain
  20. Prussion Blue
  21. Oil Red O
  22. Trichrome Stain/Reticulin
    connective tissue
  23. Congo Red
  24. Gram Stain
  25. Warthin Starry Silver
    spirochetes (syphylis, Lyme disease)
  26. Acid Fast
    -Zeihl Neelsen
    -Fite Stain
    • -mycobacterium tuberculosis
    • -M leprae
  27. Gomori Methenamine Silver
    fungi/pneumocystis carinii
  28. Periodic Acid Schiff (PAS)
    • glycogen/mucin/fungi
    • -for outlining tissue structures, basement membrane, capsules etc
  29. Wright Giemsa Stain
    peripheral smears
  30. Leukocyte Alkaline Phosphatase Stain
    differentiate CML from leukemoid rxn
  31. Tartarate Resistant Acid Phosphatase Stain
    hairy cell leukemia
  32. Myeloperoxidase
  33. Immunoperoxidase Stain
    cytokeratin, vimentin, desmin, PSA
  34. Cytopathologic Stains
    • May-Grunwald-Giemsa
    • Papanicolaou (PAP)
  35. Hyperplasia
    • increase in # of cells
    • potential for developing cancer if not treated
  36. Hypertrophy
    • increase in size of cells
    • usually occurs w/hyperplasia
  37. Atrophy
    decrease in size/function of cells
  38. Metaplasia
    replacement of 1 cell type by another
  39. Dysplasia
    disorderly growth
  40. Ex of Physiologic Hyperplasia/Hypertrophy
    breast/uterus during pregnancy
  41. Ex of Pathologic Hyperplasia
    high unopposed estrogen = endometrial hyperplasia***
  42. Labile cells
    undergo hyperplasia
  43. Stable Cells
    undergo hyperplasia/hypertrophy
  44. Permanent Cells
    undergo hypertrophy only
  45. Causes of Atrophy (8)
    disuse, denervation, reduced blood supply, indadequate nutrition, decreased hormonal stimulation, aging, occlusion of secretory ducts, pressure
  46. Lipofuscin
    • indigestible yellow-brown material left behind after cell autophagy
    • "wear and tear" pigment
  47. Agenesis
    abscence of an organ due to failure to develop
  48. Aplasia
    primordium is present but no further development
  49. Hypoplasia
    incomplete or partial development
  50. Metaplasia
    replacement of 1 adult cell type by another
  51. Squamous Metaplasia
    • columnar cells in lung replaced by squamous in order to tolerate chronic cigarette smoke
  52. Glandular Metaplasia
    • replacement of squamous by glandular epithelium
    • ex - Barrett's esophagus
  53. Connective Tissue Metaplasia
    • connective tissue in abnormal places
    • ex - sesamoid bone in muscle
  54. Myeloid Metaplasia
    • blood formation outside of bone marrow
    • ex - spleen or liver
  55. Dysplasia
    • disorderly growth/proliferation of cells
    • change in size/shape/number
    • loss of organization
    • may progress to cancer if irritant is not removed
  56. C/O
    complaining of
  57. Hypoxic Cell Injury
    inadequate oxygenation of tissue
  58. Ischemia
    decreased arterial flow to tissue
  59. Hypoxemia
    decreased amt of O2 dissolved in plasma
  60. Anemia/CO Poisoning leads to...
    decreased O2 carrying capacity of blood
  61. Consequences of Hypoxia
    • decreased ATP production
    • impaired Na-K ATPase = cellular swelling
  62. Consequences of ATP Depletion in Hypoxia
    • switch to anaerobic glycolysis for ATP
    • then depletion of glycogen
    • then accumulation of lactic acid
    • increased pH, denaturation of proteins, denatured enzymes, decreased protein synthesis, accumulation of lipid
  63. In Irreversible Cell Damage, Mt Damage Can Lead to...
    • release of cytochrome C into cytosol
    • (trigger for apoptosis)
  64. Ca2+ Role in Irreversible Cell Injury
    enzyme activation - ATPase, phopholipase, proteased, endoculeases
  65. Pyknosis
    shrinkage and darkening of the nucleus
  66. Karyorrhexis
    fragmentation and breakdown of the nucleus
  67. Karyolysis
    dissolution of the nucleus into "purple haze"
  68. Ischemia-Reperfusion Injury
    • cessation of blood flow followed by its restoration
    • may cause death of some cells via apoptosis
  69. How does reperfusion injury occur?
    • increased generation of free radicals
    • influx of Ca2+
  70. Free Radical Pathogenesis
    • 1. lipid peroxidation of membranes = increased permeability
    • 2. oxidative modification of proteins = protein fragmentation/degradation
    • 3. rxns w/thymine, thymine dimers = single stranded breaks in DNA
  71. How is Tylenol converted to a free radical?
    • cytochrome P-450 system in the liver
    • this free radical then neutralized by glutathione leading to damage to hepatocyte
    • FR damages hepatocyte cell membrane
  72. Infarction
    death of tissue due to blockage in blood supply
  73. Image Upload 1
    atherosclerotic plaque - cholesterol crystals
Card Set
Path 1 Block 1
Pathology 1, block 1 notes