Pathology Terms

  1. Branches of Pathology
    Anatomical - study of gross and microscopic changes in cells and tissues of the body caused by disease

    Clinical - measurement and identification of substances, cells and microorganisms in body fluids
  2. Surgical Pathology
    • Anatomical Pathology
    • analysis of biopsy and surgical specimens
    • EG: diagnosis of malignancy
  3. Cytopathology
    • Anatomical Pathology
    • analysis of exfoliated and aspirated cells
    • EG: Pap smear
  4. Hemopathology
    • Anatomical Pathology
    • Diagnosis of blood disorders
    • EG: lymphomas
  5. Autopsy Pathology
    • Anatomical Pathology
    • Analysis of tissues removed after death
    • EG: study for cause of death
  6. Clinical Pathology Labs
    • Urinalysis (urine)
    • Hematology (blood cell indices)
    • Chemistry (electrolytes, enzymes)
    • microbiology (bacterial culture)
    • transfusion medicine (blood typing)
  7. PAS Stain
    • glycogen, basement membranes, carbohydrate-rich molecules
    • "Pass on the carbs"
  8. Gomori Methenamine-Silver (GMS)
    Basement Membranes, fungi

    "Silver lining"
  9. Ziehl-Neelson
    Acid-Fast Bacilli (TB)

    "Jerry's got TB"
  10. Prussian Blue
    Hemosiderin (iron)
  11. Masson Trichrome
  12. Congo Red
  13. Oil Red O
  14. Ischemia
    A deficiency of blood flow to an organ or tissue
  15. Myocardial Infarction
    Tissue Necrosis caused by impairment of arterial or venous blood supply
  16. What happens after an Ischemic cell injury?
    • No O2 --> No ATP. Therefore, NA isn't pumped out and seeps in, bringing water with it. Hydropic Change
    • Less glucose, so anaerobic glycolysis increases, pH decreases. Ribosomes diss, cristae misalign
    • Ca levels rise
    • Membrane Blebbing
  17. What normally happens to ROS?
    ROS are usually reduced numerous times such that you get no superoxide formation. However, if you don't have the electrons necessary to do so, you may get an accumulation of superoxide (free radical - O2-*)
  18. Where do ROS come from?
    Endogenous sources: macrophages create, NO, neutrophils

    Exogenous Sources: radiation, drugs/toxins, pollutants
  19. Ischemia Reperfusion Injury
    • If you have an ischemia, the has been damaged and hasn't been doing it's normal functions; therefore it doesn't have the e- necessary to reduce the ROS. (you get incomplete O2 reduction)
    • If you unblock the ROS, you get a buildup of ROS that the cell can't handle, and you cause more cell injury
  20. When will you see necrosis?
    • Grossly: 18-24 hours
    • LM: 4-12 hours

    after injury
  21. What color does necrosis typically stain?
    Necrosis is typically more eosinophilic (less nuclei)
  22. Pyknosis
    Nuclear shrinkage
  23. Karyorrhexis
    Nuclear Fragmentation
  24. Karyolysis
    Nuclear Dissolution
  25. Coagulative Necrosis
    • Still see structure, but no nuclei
    • Caused by Ischemia
    • Eosinophilia is a typical feature
  26. Liquefactive Necrosis
    • Seen in two distinct conditions:
    • 1) Ischemia in the brain (stroke)
    •     autolysis is dominant
    • 2) Abscess formation just about anywhere in the body
    •     PMNs everywhere
  27. Gangrene
    • Dry - a form of coagulative
    • Wet - bacterial infection on top of necrosis
    • Gas - results from puncture wound infection
  28. Caseous Necrosis
    • Cheeeeeese
    • Can only use this to describe it grossly.

    otherwise, we're looking at a granuloma
  29. Fat Necrosis
    • Two Types:
    • 1) Enzymatic: in pancreas after acute inflammation. leakage of pancreatic ducts causes digestive enzymes to attack local fat cells. You see "ghost cells" that are more basophilic.
    • 2) non-Enzymatic: "trauma fat necrosis"
  30. Fibrinoid Necrosis
    • Vessel damage dueto malignant hypertension, autoimmune disease. 
    • The site is very eosinophilic
  31. Apoptosis
    • ATP-dependent planned cell death.
    • Intrinsic: Cytochrome C leakage
    • Extrinsic: Death-receptor mediated.

    Affects single cells
  32. Autophagy
    • 'eating yourself'
    • Can lead to apoptosis
  33. Steatosis
    • Fatty Change
    • Intracellular accumulation 
    • Acute: microvesicular, drugs/toxins, fatty acids, response to drugs/toxins. life-threatening
    • Chronic: macrovesicular, alcohol, triglycerides, response to alcohol. reversible
  34. Mallory Bodies
    • Normal in cell, upregulated in response to injury
    • Intracellular protein accumulation
    • Heat Shock Proteins + Intermediate Filaments
    • Attempts to re-fold or stabilize damaged proteins to avoid intermediate aggregation
    • Hyaline
  35. Hyaline
    Homogenous, glassy, pink material
  36. Hemosiderin
    • Intracellular Pigment Accumulation, heme derived
    • Storage form of Iron
    • Hemosiderosis: short term harmless accumulatoin
    • Hemochromatosis: long term w/ harm to cell. 
    •    Primary: Hereditory, increase in intenstinal    iron absorption due to mutation
    •    Secondary: multiple causes, esp blood         transfusions
  37. Heart Failure Cells
    Localized macrophages containing hemosiderin in the lungs. Indicate heart failure
  38. Cirrhosis
    Regeneration Nodule + Fibrosis

    See it as hemochromatosis
  39. Bilirubin
    • Intracellular Pigment Accumulation: Heme-derived
    • Transported bound to albumin, brought to liver for conjugation to form water-soluble form
    • Yellow color
    • Jaundice if deposits in skin
  40. Carbon Accumulation
    Intracellular Pigment Accumulation - Exogenous
  41. Amyloidosis
    • Interstitial Accumulation
    • An aggregation of misfolded amyloid proteins. Two beta pleated sheets
    • Amyloid Light Chain: plasma cell Ig-secreting neoplasms
    • Amyloid Assosciated: derived from precurser to serum amyloid A protein. Released as part of acute inflammation
    • Congo red stain
  42. Calcification
    • Interstitial Accumulation
    • Metastatic: High serum Ca, normal Tissue. Diffuse all over the place
    • Dystrophic: Normal serum Ca, abnormal Tissue. Locallized
  43. 5 Cardinal Signs of Acute inflammation
    • 1) Swelling
    • 2) Redness
    • 3) Heat
    • 4) Pain
    • 5) Loss of function

    Redness + Heat = Erythema
  44. Erythema
    Redness + Heat (cardinal signs of acute inflammation)
  45. What are the five hemodynamic events of acute inflammation?
    • 1) Transient vasoconstriction of arterioles: "knee jerk reaction" - may not occur. Thromboxane
    • 2) Vasodilation of arterioles: hydrostatic pressure >> colloid pressure, so net flow will not become out of vessel. This leads to...
    • 3) Hyperemia: increased amount of blood in tissue (Edema is increased ISF)
    • 4) Change in capillary permeability: mediated by histamine and seratonin. Leads to more outflow and edema
    • 5) Formation of Exudate
  46. Hyperemia
    Increased amount of blood in tissue
  47. Edema
    Increased Instersitial fluid
  48. Role of serotonin and histamine in acute inflammation?
    Mediate the initial response for increase capillary permeability in the hemodynamic events of acute inflammation. Increase in capillary permeability leads to edema and increased hydrostatic pressure
  49. Types of Edema
    • Edema is water and electrolytes
    • Exudate (>1.5 g/dL)
    • Transudate (< 1.5 g/dL)
  50. Types of Exudates
    • 1) Fibrinous: increase in fibrin. Ex: fibrinous pericarditis
    • 2) Serous: fluid-filled. Ex: inflammation following a burn
    • 3) Serosanguineous/Sanguineous: bloody
    • 4) Purulent: Pus. basically a fibrinous exudate + many inflammatory cells
  51. What happens to blood flow in acute inflammation?
    • Viscosity increases because of increase in cell concentration (hemoconcentration)
    • blood flow slows down (stasis) and becomes so packed that you can actually see it in slides (vascular congestion)
  52. Hemoconcentration
    The increase in blood cell concentration due to fluid loss in acute inflammation
  53. Stasis
    Slowing of blood flow in acute inflammation. Due to hemoconcentration
  54. Vascular Congestion
    Due to hemoconcentration, blood vessels become so packed that you can see them packed full of cells in histological slides
  55. What happens to lymphatics in acute inflammation?
    • Lympathic drainage increases to drain the edema
    • Lymphangitis: lymphatics become inflammed
    • Lymphandenitis: Lymph nodes become inflammed
  56. Lymphangitis
    inflammation of lymphatics in acute inflammation
  57. Lymphandenitis
    Inflammation of lymph nodes in acute inflammation
  58. What are the cellular events in acute inflammation? (Recruitment of cells from blood stream)
    • My Poor Disease Can't Proliferate
    • Margination: because of increased viscosity, WBCs get pushed to periphery
    • Pavementation: light binding to epithelial cells (selectin - light, intergrins - loose)
    • Diapedesis: change in cell morphology that let's it migrate through epithelial cells to inflammation
    • Chemotaxis: gradients/chemicals direct cell where to do
    • Phagocytosis
  59. Margination
    • Part of cell recruitment in acute inflammation
    • WBCs get pushed to periphery due to increase in viscosity
  60. Pavementation
    • Part of cell recruitment in acute inflammation
    • Binding of cell to epithelial cells (selectins-light. Integrins - tight)
  61. Diapedesis
    • Part of cell recruitment in acute inflammatoin
    • Change in cell morphology to allow it to pass through epithelial cells
  62. Chemotaxis
    • Part of cell recruitment in acute inflammation
    • Gradients/chemicals tell cells where to go once out of blood stream
  63. Cells of acute inflammation
    • PMNs are most important
    • Macrophages start to appear after 24/48 hours, and take over as the dominant cell type at around day 5, as chronic starts
    • Eosinophils
    • Mast cells - mediate inflammatory response (histamine and heparin)
    • Lymphocytes
  64. Laboratory Evidence of Acute Inflammation
    • Looking for increased leukocyte concentration in the blood
    • Leukocytosis: increased leukocytes in blood (more lymphoctes and neutrophils)
  65. Leukocytosis
    • Increased leukocytes in blood
    • Lymphocytosis: increased lymphocytes
    • Neutrophilia: increased neutrophils
  66. Leukopenia
    • Decreased leukocytes in blood
    • Lymphopenia: decreased lymphocytes in blood
    • Neutropenia: Decreased neutrophils in blood
  67. Bullae
    A vesicle > 5mm in diamter. filled w/ exudate, probably serous
  68. Eschar
    slough produced by chemical or thermal burns, or gangrene
  69. Furuncle and Carbuncle
    • Localized inflammation and ulcer of the skin, usually in hairy area
    • A carbuncle is a shit ton of furuncles, will see erythema and swelling
  70. Erysipelas and Cellulitis
    • Erysipelas: A spreading infection of the dermis which produces a raised, red, painful lesion of skin
    • Cellulitis: A spreaking inflammation of the subcutaneous connective tissues
  71. Cytokines to activate macrophages/mediators of chronic inflammation
    • IFN-Gamma from T Cells, IL-4 from others
    • TFN is most important mediator of chronic: without it, granuloma doesn't form
  72. TFN
    Most important mediator of chronic inflammation. Without it, granulomas do not form
  73. IFN-Gamma
    Macrophage activation by T cells
  74. Morphological Features of Acute Inflammation
    PMNs, Exudate
  75. Morphological Hallmarks of Chronic Inflammation
    Mononuclear cells (giant cells in granuloma), fibrosis
  76. Types of Giant cells
    • Langhan (horseshoe)
    • Asteroid Body
    • Schaumann Body
  77. Cells in a granuloma
    • Granuloma made around indigestible material
    • epithelioid cells in center, mononuclear cells make ring. 
    • Will sometimes see thick fibrous ring as well
    • Giant cells
  78. Eotaxin
    Causes eosinophelia, which normally happens in the course of Acute on Chronic inflammation
  79. Necrotizing Granuloma
    What it looks like, an example
    • No nuclei in center
    • Tuberculosis
  80. Non-necrotizing Granuloma
    What it looks like, example
    • Nuclei in center.
    • Saroidosis
  81. Acute on Chronic Inflammation - how? what you expect to see
    • usually infection before first one clears.
    • eosinophilia (eotaxin)
  82. Morphology of Healing
    Looking for macrophages, angiogenesis, fibroblasts
  83. Resolution wrt healing
    Resolution is restoration to pre-injury state
  84. Regeneration wrt healing
    • Regeneration is replacement of lost cells by cells of the same type
    • May result in loss of function
  85. Repair wrt healing
    • Repair is replacement of cells to connective tissue (fibrosis)
    • May result in loss of function
  86. Organization - what is it and when does it happen?
    • the conversion of dead tissue or inert material into granulation tissue.
    • happens in fibrinous exudates, thrombi, infarcts, wounds
  87. Granulation Tissue
    • Light pink and softly granular grossly
    • Contains macrophages, fibroblasts, new vessel formation, mast cells
    • Presence of granulation tissue means healing is taking place
  88. Primary Union (First Intention)
    • occurs with "clean cuts"
    • minimal myofibroblast activity
  89. Secondary Union (second intension)
    • Happens when wound edges can't be matched
    • Lots of myofibroblast activity
Card Set
Pathology Terms
Terms and concepts for Pathology: Effects of Injury on Tissues I & II Intro to Path Inflammation and Healing I,II,III