Pathology Midterm I

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  1. (Appearance of lesions in soft tissue)

    Macule
    An area with a color different from the surrounding tissue; flat; less than 1 cm. Ex: freckle
  2. Patch
    Same criteria as macule (area w/ different color), but greater than 1 cm.
  3. Papule
    A circumscribed elevated or protruding lesion that is less than 1 cm. Ex: mole
  4. Nodule
    A circumscribed elevated or protruding lesion that is greater than 1 cm.
  5. Vesicle
    An elevated, fluid-filled lesion less than 1 cm in size.
  6. Bulla
    An elevated, fluid-filled lesion greater than 1 cm in size.
  7. Pustule
    Vesicle or bulla containing pus.
  8. Sessile
    Describing the base of a lesion as broad or flat.
  9. Pedunculated
    Attached by a stem or stalk base.
  10. Lobule
    A segment or lobe that is part of the whole.
  11. (color/size of lesions)

    Color
    Red, pink, salmon, white, blue-black, gray, brown, purple, black.
  12. Erythema
    An abnormal redness of soft tissues.
  13. Pallor
    Paleness of skin or mucosa.
  14. (consistency)

    Indurated
    Firm, hard to palpation.
  15. Fluctuant
    Fluid-filled, soft (blister like).
  16. Mobile
    Lesion moves when palpated.
  17. Fixed
    Non-mobile, matted.
  18. (surface texture)

    Corrugated
    Wrinkled.
  19. Papillary
    Multiple projections/elevations found in clusters.
  20. Fissured
    A cleft or groove.
  21. (Variants of normal)

    Retrocuspid papilla
    Small mucosal tags on the lingual.
  22. Varicosities
    Aquired vascular proliferation under the tongue.
  23. Linea alba
    "White line."
  24. Leukoedema
    White-bluish tinge of the buccal mucosa.
  25. Lingual thyroid
    • (Benign condition)
    • Ectopic thyroid tissue
  26. Fissured tongue
    • (Benign condition)
    • Deep grooves/cracks in tongue
  27. Median rhomboid glossitis
    • (Benign condition)
    • Reddish patch/plaque @ the midline dorsum of the tongue
  28. Benign migratory glossitis
    (Geographic tongue)
    • (Benign condition)
    • Patchy appearance of the tongue with desquamation of filliform papilla; "pattern changes."
  29. Hairy tongue
    • (Benign condition)
    • White or black
    • Elongated/lengthened papillae
  30. Inflammation and its benefits
    • A nonspecific response to injury.
    • -localize and isolate injured/infected area
    • -neutralize and inactivate toxic substances
    • -destroys/limits growth of infecting organisms
    • -prepares tissue for healing/repair
  31. Local clinical signs of inflammation
    • Redness (rubor- from dilation)
    • Heat (calor- temp change)
    • Swelling (tumor- vessel permeability)
    • Pain (dolor- pressure on nerves)
    • Loss of normal tissue function (function laesa)
  32. Systemic clinical signs of inflammation
    • Fever (pyrogens trigger hypothalamus to increase temp)
    • C-reactive protein (liver protein elevated)
    • Lymphadenopathy/lymphadenitis (from increased number or increased size of cells)
    • Leukocytosis (increased # of WBCs, 10,000-30,000/cc)
  33. Microscopic signs/steps of inflammation
    • 1. Immediate constriction
    • 2. Dilation of the same vessels via histamine, produces hyperemia, erythema, and heat
    • 3. Increased permeability, leads to edema
    • 4. Blood viscosity increases, flow decreases
    • 5. Margination
    • 6. Pavementing
    • 7. Emigration
    • 8. Chemotaxis
    • 9. Phagocytosis
  34. Serous fluid vs. purulence (pus)
    • Serious: plasma fluids and proteins, with few WBCs
    • Purulence: tissue debris, many WBCs, fluid, and proteins
  35. Margination
    Movement of WBCs to the periphery of the vessel caused by chemotactic factors (1st step)
  36. Pavementing
    WBCs line blood vessels via electronegative factors (2nd step)
  37. Emigration
    Movement of WBCs from the blood vessel and through the vessel wall (3rd step)
  38. Chemotaxis
    Directed movement to the site of injury with chemotactic factors (4th step)
  39. Phagocytosis
    WBCs digest foreign substances from injured site by ingesting them (5th step)
  40. Acute inflammation
    • Initial response to the tissue to an irritant/harmful stimuli
    • SHORT DURATION-few days
    • Tissue regenerates to original self
  41. Chronic inflammation
    • LONG DURATION-weeks, months, indefinitely
    • Occurs in the injury continues
    • Caused by persistent injury/unresolved acute inflammation; may also be caused by certain viral infec/autoimmune diseases
  42. Associated with chronic inflammation
    • Granulomatous inflammation: collections of macrophages around the injury the form granuloma-like tissue
    • Mulinucleated giant cells
  43. Cells involved in acute/chronic inflammation
    • ACUTE: 6 types of leukocytes (WBCs)
    • 1. Neutrophils (PMNs)
    • 2. Mast cells
    • 3. Macrophage
    • 4. Eosinophils
    • 5. Basophils
    • 6. Lymphoctyes

    CHRONIC: macrophages, lymphocytes, plasma cells, fibroblasts, and neutrophils.

    NOTE: degrees of inflamm are transitional. Acute/chronic signs may be observed concurrently.
  44. Neutrophils (PMNs)
    • First cell to emigrate to site of injury/prominent cell involved in ACUTE inflammation
    • 60-70% of all WBCs
    • Contain lysosomes (granules w/in WBC) that contain enzymes able to destroy foreign substances.
  45. Mast cells
    Contain histamine and anticoagulant
  46. Macrophage
    • SECOND CELL involved in inflammatory process
    • *monocyte when circulating in blood, macrophage in tissue
    • 3-8% of all WBCs
    • Major role in IMMUNE response
  47. Eosinophils
    • Primarily involved in inflamm assoc with ALLERGIES, CT
    • Parasitic infections
  48. Basophils
    Allergy and antibody response-released histamine
  49. Lymphocytes
    • T cells (produced in the thymus)- chronic inflammation and immune response
    • B cells (plasma cells, produced in lymphoid tissue)- assist T cells, responsible for antibody production.
  50. Describe chemical mediators of inflammation
    • Agents that can start or amplify inflammation
    • Cell derived or plasma protein derived substances
    • Produced by elements in blood, WBCs, and pathogenic organisms
  51. What are some chemical mediators of inflammation and what do they do?
    • Prostaglandins, lysosomal enzymes, and endotoxins
    • Induce inflammation and produce the signs of edema, erythema, fever, and pain

    **Three plasma protein systems primarily involved
  52. What are the three plasma protein systems primarily involved in chemical mediation of inflammation?
    • The Kinin System
    • Advances by substances (proteins) present in plasma
    • Induces pain
    • Bradykinin is the primary kinin- SM contraction, dilation, and permeability

    • The Clotting Mechanism
    • Primary function: form clots @ the site of injury
    • Fibrinogen, prothrombin, plasminogen, factor VIII
    • Mediates inflammation with the kinin

    • The Complement System
    • Cause mast cells to release biochemical histamine granules
  53. What is the goal of all inflammatory processes?
    Repair

    • -destroyed cells replaced by new cells
    • -functioning cells often replaced by scar
    • -repair process takes approx. 2 weeks for healing
  54. Describe the day of injury
    • Clot forms as a collection of RBCs, platelets (thrombocytes, play critical role in clot), fibrin
    • Platelets affected by asprin, NSAIDS, alcohol, kidney disease.
  55. Describe the day after injury
    Acute inflammation dominates

    (neutrophils- phagocytosis)
  56. Describe day 2 after injury
    • Macrophages increase in #, phagocytosis continues
    • Fibroblasts produce new CT (granulation tissue)
    • Epithelial cells migrate across fibrin clot
  57. Describe day 7 after injury
    • Fibrin is digested by enzymes
    • Skin surface = red b/c dilation, increased perm, and thinness of skin
  58. Describe day 14 after injury
    • Tissue is remodeled and tissue strength approaching normal
    • Scar formation is dependent on depth of injury
  59. Primary intention (types of repair)
    • Direct healing of one skin edge to another (surgical incision w/ sutures)
    • Minimal scar due to direct healing
  60. Secondary intention (types of repair)
    • Indirect healing w/ formation of granulation tissue and loss of normal tissue
    • Increased scar formation
  61. Tertiary intention (types of repair)
    • Delayed primary intention
    • (ex. waiting for an infection to resolve)
  62. Bone repair (types of repair)
    Granulation tissue followed by immature bone formation then organized bone develops
  63. Attrition
    • Wearing away of tooth structure
    • Most often occurs on the occlusal surface

    *Bruxism: attrition caused by clenching or grinding
  64. Abrasion
    Wearing away of tooth structure resulting from a mechanical action (ex. toothbrush scrubbing w/ excessive pressure)

  65. Abfraction
    • Wedge shaped lesions @ the cervical 1/3
    • Already weakened tooth structure = easily affected
  66. Erosion
    • Chemical wearing of tooth structure
    • Acidic oral environment (can occur facial/lingual)
  67. Meth abuse
    • Rapid erosion of teeth
    • B/c acid content of meth, xerostomia, high sugar liquid craving, lack of OH
  68. Phenol burn
    • Used in dentistry as a cavity sterilizing agent and a cauterizing agent
    • Will cause whitening and sloughing of the area as a result of tissue destruction
  69. Asprin burn
    Occurs when asprin is allowed to rest on the oral mucosa w/o swallowing (ex. placed directly on canker sore)
  70. Hematoma
    Caused by trauma, no tx required
  71. Fictional keratosis
    • Caused by chronic rubbing of the tissue resulting in an opalescent, keratotic tissue
    • Not malignant
    • Local cause
    • Not the same as leukoplakia
    • Example: linea alba
  72. Nicotine stomatitis
    • Keratotic, opalescent palatal tissue
    • Reddish raised dots w/in the keratosis-inflammed minor salivary glands
    • Heavy smokers
  73. Tobacco pouch keratosis
    • Smokeless tobacco use
    • Ridges of keratotic tissue where the tobacco is placed
    • "Dry river bed" appearance
  74. Mucocele
    Minor salivary gland obstruction
  75. Ranula
    • Major salivary gland obstruction
    • Location: sublingual
  76. Sialolith
    • Salivary gland stone
    • Assoc. w/ salivary glad obstruction
    • Resulting condition: Sialadenitis
  77. Pyogenic granuloma
    • CT and BV tumor
    • Not pus producing
    • Treat w/ surgical excision
  78. What is also known as a pregnancy tumor?
    Pyogenic granuloma
  79. Giant cell granuloma
    • Multi-nucleated giant cells
    • RBCs and inflamm cells present
    • May be peripheral or central
    • Cause is unclear
    • Tx surgical excision
  80. Fibrous hyperplasia
    Typically caused by dentures

  81. What is epilus fissuratum also known as
    fibrous hyperplasia
  82. Periapical granuloma
    • Chronic inflammatory tissue @ apex of nonvital tooth
    • Granulation tissue containing epithelial rest of malasez 
    • Tx RCT or extraction
  83. Radicular (PA) cyst
    • Most common cyst
    • Epithelial lined
    • Nonvital tooth
    • Tx RCT or extraction and curettage
  84. Residual cyst
    • Cyst that remains after an extraction
    • No tooth is present
  85. Focal sclerosing osetomyelitis
    • Apex of tooth
    • May be caused by a reaction to an infection
    • No tx
  86. What is condensing osteitis also known as?
    focal sclerosing osteomyelitis
  87. Resorption
    • Breakdown and destruction of tooth structure
    • May be a result of trauma/stress to structure
    • Etiology may be unknown
  88. What does the immune response do?
    • Defends the body from pathogens
    • Has capacity to remember previous infection/respond quicker
    • Consists mainly of lymphocytes/plasma cells
    • Can cause increased injury and repair
    • Innate or aquired
  89. Innate immune response
    • WHAT YOU'RE BORN WITH- genetic ability of body to protect against a specific pathogen
    • Body's natural resistance- response to an injury WITHOUT CELL MEMORY
    • Response takes hours and is NONspecific to a foreign body
  90. Acquired/adaptive immune response
    • Body's response to injury/insult when cells recognize/REMEMBER the foreign body from a prior exposure
    • Natural or artificial
    • Response is SPECIFIC to a foreign body
  91. Stages of the acquired immune response
    • 1. B and T cells recognize the foreign body
    • 2. Cells are activated to reproduce (clone) and change (differentiate) into cells that can respond to the antigen
    • 3. Some cells produce antibodies, others work at eliminating the antigen
    • 4. Antigens eliminated, memory cells remain with ability to respond if antigen return
    • 5. Response takes DAYS
  92. Antigen
    • Any substance that stimulates the body's immune defenses
    • Body sees substance as foreign, triggers production of antibodies to defend against substance in future exposure
    • (antibody generators)
  93. Cause of autoimmune disorders
    The body's reaction to its own antigens
  94. What are antibodies also known as?
    Immunoglobulins (Igs)
  95. What are antibodies?
    • Gamma globulin proteins w/ role of recognizing/neutralizing foreign substances
    • Generated by plasma cells as response to specific antigen
    • Trigger mast cells
  96. What are the five types of antibodies?
    • 1. IgM
    • 2. IgA
    • 3. IgG
    • 4. IgE
    • 5. IgD
  97. IgM
    • Basic antibody
    • 1st antibody to respond to antigen exposure
    • May be present prior to exposure- "natural antibody"
    • Largest antibody
  98. IgA
    • Protects body fluids
    • Secretory: saliva, tears, genitourinary tract, gastrointestinal
    • Serous: blood
  99. IgG
    • Involved in secondary response
    • Most abundant antibody
    • Only antibody to cross placenta (passive immunity for baby)
  100. IgE
    • Response to specific allergens, especially type I hypersensitivity reactions
    • Rarest antibody
  101. IgD
    • Activates B lymphocytes
    • Specific role is unknown
  102. What is the primary cell involved in the immune response?
    • Lymphocyte (special kind of leukocyte)
    • Recognize and respond to an antigen
    • 20-30% of all WBCs
  103. What are the three types of lymphocytes?
    • 1. B lymphocytes
    • 2. T lymphocytes
    • 3. NK cells
  104. Humoral immunity
    • B lymphocytes: primary cell
    • Involves production of antibodies
    • Type 1, 2, 3 hypersensitivity reactions
  105. Cell-mediated immunity
    • T lymphocytes are primary cells
    • Type IV hypersensitivity reaction

    **Humoral and cell mediated responses are interrelated
  106. B lymphocytes
    • Component of acquired/adaptive immunity
    • 10-15% of lymphocytes
    • Produced by stem cells in bone marrow (T lymphocyte is also)
    • Matures in lymphoid tissure- lymph nodes, tonsillar tissue, etc.
    • Ivolved in humoral immune response
    • When activated, cells migrate to site of pathogen and presents antigen to T cell, triggering T cell activity
  107. What are the two types of B lymphocytes?
    • 1. Plasma cells- produce proteins called antibodies (Ig)
    • 2. B memory cells- remembers the antigen
  108. T lymphocytes
    • 80% of all lymphocytes
    • Mature in thymus gland
    • Involved in Cell mediated immune response
    • Carry receptors to recognize specific targets
    • 4 types of T cells with having a different immune response
    • Communication of cells is by lymphokines

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Pathology Midterm I
Updated:
2016-01-24 06:09:47
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