Stress inflammation immunity

  1. Natural barriers and the inflammatory response
    Innate resistance
  2. Physical and mechanical barriers. Linings of GI GU resp tracts. Highly interconnected junctions. Sloughing off of cells. Coughing and sneezing. Washing vomiting urinating. Mucus and cilia
    First line of defense
  3. Antibacterial peptides in mucus, perspiration (sweat), saliva, tears, ear wax. Cathelicidins, defensins, and collectins
    Biochemical barriers, and antimicrobial peptides
  4. 3rd line of defense
    Adaptive acquired immunity
  5. Inhibits colonization by pathogens, releases chemicals that prevent infection
    Normal microbiome

    Examples: vaginal (lactobacillus), intestinal (ammonia, phenois, indoles)
  6. Second line of defense
    Inflammatory response
  7. Cardinal signs of inflammatory response (4)
    Redness. Heat
  8. Blood vessel dilation, increased vascular permeability and leakage, white blood cell (WBC) adherence to the inner walls of the vessels, and migration through the vessels. Limit and control the inflammatory process. Prevent and limit infection and further damage. Interact with components of the adaptive immune system. Prepare the area of injury for healing.
    vascular inflammatory response
  9. migration through the vessels
  10. provide a biochemical barrier against invading pathogens are the
    protein system
  11. inactive enzymes
  12. First proenzyme is converted to an active enzyme. The activation of the first component of a system results in sequential activation of other components.
    Sequentially activated cascade
  13. Can destroy pathogens directly Activates or collaborates with every other component of the inflammatory response. Anaphylatoxic activity resulting in mast cell degranulation; leukocyte chemotaxis; opsonization; cell lysis
    complement system
  14. Antibodies and antigens in complement system
    classical pathways
  15. Mannose-containing bacterial carbohydrates in complement system
    lectin pathways
  16. Gram-negative bacterial and fungal cell wall polysaccharides in complement system
    alternative pathways
  17. Plasma protein system that Forms a fibrinous mesh at an injured or inflamed site Prevents the spread of infection. Keeps microorganisms and foreign bodies at the site of inflammation for removal.  Forms a clot that stops the bleeding. Provides a framework for repair and healing.
    Clotting (coagulation) system
  18. main substance of clotting coagualation system
  19. in clotting coagulation system Is activated by the tissue factor outside the vascular space.
    extrinsic pathways
  20. in clotting coagulation system Is activated in the vascular space when the vessel wall is damaged.
    intrinsic pathways
  21. Functions to activate and assist inflammatory cells. primarily bradykinin, degraded by kininases, case dilation of blood vessels, pain, smooth muscle contraction, vascular permeability, and leukocyte chemotaxis
    kinin system
  22. 2 mechanisms are available to either activate or inactivate (regulate) these 3 plasma protein systems (clotting cascade, complement system, kinin proteins)
    • plasma-activates mechanism
    • hageman factor-activates mechanism
  23. Carboxypeptidase Inhibits
    C3a and C5a
  24. histaminase and arylsulfatase inhibits
  25. kinases inhibits
  26. C1 esterase inhibitor inhibits
  27. Mast cells Granulocytes (neutrophils, eosinophils, basophils) Monocytes and macrophages Natural killer (NK) cells and lymphocytes Cellular fragments (platelets) are all examples of
    cellular mediators
  28. Are responsible for vascular changes. Modulate the localization and activities of other inflammatory cells.nInclude histamine, chemotactic factors, leukotrienes, prostaglandins, and the platelet-activating factor.
    biochemical mediators
  29. most important activators of inflammation
    mast cells
  30. Cell surface or cellular receptors Pattern recognition receptors (PRRs): Recognize pathogen-associated molecular patterns (PAMPs).
    toll like receptors (TLRs)
  31. Cell surface or cellular receptors Pattern recognition receptors (PRRs): recognize complement fragments
    complement receptors
  32. Cell surface or cellular receptors Pattern recognition receptors (PRRs): promote phagocytosis
    scavenger receptors
  33. cell surface / receptors damage associated
    molecular patterns
  34. Is initiated when tissue injury occurs or when PAMPs are recognized by PRRs (pattern recognition receptors) on cells of the innate immune system.
    inflammatory response
  35. cellular products that Regulate innate or adaptive resistance by affecting other neighboring cells. synergistic or antagonistic, proinflammatory and antiinflammatory. includes interleukins, interferons, and tumor necrosis factor (TNF). (2)
    chemokines, ctyokines
  36. chemokines or cytokines actions are ______ : The same molecule may have a large variety of different biologic activities, depending on the particular target cell to which it binds.
  37. Are produced primarily by macrophages and lymphocytes in response to a microorganisms or stimulation by other products of inflammation. Help regulate inflammation
    interleukins (ILs)
  38. IL (interleukin) 1 is a ______ cytkine that causes _____
    proinflammatory, fever
  39. IL 6 is _____ cytokine that helps with ____
    proinflammatory; healing
  40. 2 antiinflammatory cytokines
    IL 10 and TGF-B (transforming growth factor-beta
  41. nProtects against viral infections. Is produced and released by virally infected host cells in response to viral double-stranded ribonucleic acid (RNA). Does not directly kill viruses but prevents them from infecting additional healthy cells.
    Interferons (INFs)
  42. Type of interferon that produces antiviral prorteins (2)
    INF-a and INF-b
  43. Type of interferon that increases microbiocidal activity of macrophages
  44. Cytokine that Is secreted by macrophages in response to PAMP by TLR recognition. Produces local and systemic effects. Induces fever by acting as an endogenous pyrogen. Increases synthesis of proinflammatory proteins. Causes muscle wasting and intravascular thrombosis. Is probably responsible for fatalities from shock caused by gram-negative bacterial infections.
    TNF - alpha or tumor necrosis factor
  45. Another word for muscle waisting
  46. Induce WBC chemotaxis.nAre produced by macrophages, fibroblasts, and endothelial cells. More than 40 different kinds exist.
  47. chemokine that affect monocytes, lymphocytes, eosinophils
  48. Chemokine that affect neutrophils
    CXC chemokine
  49. Are cellular bags of granules located in loose connective tissues close to blood vessels. Skin, digestive lining, and respiratory tract. Activation by Physical injury, chemical agents, immunologic processes, and TLRs (toll like receptors)
    Mast cells
  50. Mast cell chemicals are released in two ways
    1.Degranulation 2.Synthesis of lipid-derived chemical mediators
  51. Releases histamine which Causes temporary and rapid constriction of the large blood vessels and dilation of the postcapillary venules. Endothelial cells that line the capillaries are retracted.
    mast cell degranulation
  52. mast cell degranulation receptor present in smooth muscle cells of the bronchi. Induces bronchoconstriction. proinflammatory
    h1 receptor
  53. mast cell degranulation receptor Is present on parietal cells of the stomach mucosa. Induces the secretion of gastric acid. antiinflammatory
    h2 receptor
  54. Attract neutrophils and eosinophils of anaphylaxis (ECF-A)
    chemotactic factors
  55. Cellular and humoral responses (are/arenot) independent. Humoral immunity is ____ with a ___ antibody. and cell-mediated immunity is ______ differentiation
    are not, fluid, circulating

    T cell
  56. Are the product of arachidonic acid from mast cell membranes. Have similar effects to histamine. Are more important in the later stages of inflammation.
  57. Have similar effects to leukotrienes; they also induce pain.
  58. Effect is similar to leukotrienes; they also activate platelets.
    platelet-activating factor
  59. maintains normal blood flow, produces nitric oxide (NO) and prostacyclin (PGI2). During inflammation it expresses receptors that help leukocytes leave circulation, retracts to allow fluid to pass into tissues, if damaged it promotes clotting
  60. maintain blood flow and pressure and inhibit platelet activation (2)
    NO and PG12
  61. Maintans vascular tone
    NO (nitric oxide)
  62. Are cellular fragments formed from megakaryocytes, are also called thrombocytes. Activation stops bleeding and degranulation, contain alpha and dense granules.
  63. a phagocyte Predominate in early inflammatory responses. Ingest bacteria, dead cells, and cellular debris. Are short lived and become components of the purulent exudate (pus). Removal of debris in sterile lesions and Phagocytosis of bacteria in nonsterile lesions
    neutrophils or polymorphonuclear neutrophils
  64. Phagocyte that Provide the defense against parasites and regulate vascular mediators. Help control vascular effects of inflammation.
  65. Phagocytes Are similar to but are not mast cells. Are an important source for cytokine IL-4. Are associated with allergies and asthma. Their role is uncertain.
  66. phagocyte that are produced in the bone marrow, enter circulation, migrate to the inflammatory site, and develop into macrophages. are precursors to macrophages in tissues

    Kupffer cells (liver);
    alveolar macrophages (lungs);
    and microglia (brain)
  67. larger than monocytes, are more active than phagocytes, and are important cellular initiators of inflammation; they help in wound healing. Activation results in increased phagocytic activity, size, plasma membrane area, glucose metabolism, and number of lysosomes; they predominate in late inflammation.
  68. phagocytes that Recognize and eliminate cells that are infected with viruses and cancer cells in the blood.
    NK cells
  69. phagocytes that are the main component of adaptive immune response
  70. Is the process by which a cell ingests and disposes of foreign material. Is the destruction of microorganisms and cellular debris. Production of adhesion molecules occurs.
  71. during phagocytosis leukocytes adhere to endothial cells (2 names)
    margination or pavementing
  72. during phagocytosis, cells emigrate through the endothelial junctions
  73. ˜result from vascular changes and corresponding leakage of circulating components into the tissue.
  74. 2 manifestations of inflammation From vasodilation and increased blood flow
    heat and redness
  75. Severe manifestation of inflammation
    loss of function
  76. Manifestations of inflammation From exudate accumulations and fluid from capillary permeability
  77. Manifestations of inflammation From pressure exerted by exudate accumulations, prostaglandins, and bradykinins
  78. Functions of inflammation: Dilute ___, carry plasma ____ and _____ to injury site, carry bacterial _____ and ____ away from site
    toxins, proteins, leukocytes, toxins and debris
  79. Fluid and cells such as protein and debris
  80. Watery exudate: Indicates early inflammation
  81. Thick, clotted exudate: Indicates more advanced inflammation
  82. Pus exudate: Indicates a bacterial infection in exudate (2 names)
    purulent / suppurative
  83. Exudate containing blood: Indicates bleeding.
    Hemorrhagic exudate
  84. Caused by exogenous and endogenous (IL-1) pyrogens. Acts directly on the hypothalamus
  85. Increased numbers of circulating leukocytes, Left shift, increase in immature cells (bands)
  86. Acute-phase reactants, C-reactive protein, fibrinogen, haptoglobin, amyloid A, and ceruloplasmin are all caused by ______
    increased plasma protein synthesis
  87. Is inflammation that lasts from 2 weeks to months to years. Is often related to an unsuccessful acute inflammatory response. Other causes are High lipid and wax content of a microorganism Ability to survive inside the macrophage, Toxins, Chemicals, particulate matter, or physical irritants
    chronic inflammation
  88. Dense infiltration of lymphocytes and macrophages, Granuloma formation, Epithelioid cell formation, Giant cell formation are all examples of
    chronic inflammation
  89. resolution and repair most favorable outcome
  90. returning injured tissue to original structure and fuction
  91. replacement of destroyed tissue with scar tissue
  92. Primarily composed of collagen to restore the tensile strength of the tissue
    scar tissue
  93. Cleaning up dissolved clots, microorganisms, erythrocytes, and dead tissue cells
  94. filling in the wound
  95. sealing the wound
  96. shrinking the wound
  97. Wounds that heal under conditions of minimal tissue lossnOriginal tissue structure and function that have been restored are _____ intention healing
  98. Wounds that require significantly more tissue replacement, like Open wounds, Wounds that cause scar formation need _____ healing intention
  99. Healed wound is remodeled. This phase begins several weeks after injury and may last for 2 years. Cellular differentiation continues. Scar tissue forms. Scar remodeling occurs.
    maturation phase
  100. Hemorrhage Fibrous adhesion Infection Excess scar formation Wound sepsis Hypovolemia Hypoproteinemia Antiinflammatory steroids are all examples of
    dysfunction during inflammatory response
  101. T helper lymphocytes (differences based on cytokine production)

    ______ provide help in cell mediated immunity

    ______ provide help in developing humoral immunity

  102. Causes malnutrition, keloids, hypertrophic scar
    impaired collagen matrix assembly
  103. Caused by Antiinflammatory steroids, hypoxemia, and nutritional deficienciesnCleaning with povidone-iodine and hydrogen peroxide
    impaired epithelialization
  104. Results from excessive myofibroblast derived tension
    impaired contraction or contractures
  105. Wound pulls apart at the suture line.Causes: Excessive strain, wound sepsis, and obesity Occurs 5 to 12 days after suture. Characteristics Serous drainage is increased. Feels like something “gave way.”Surgery is required.
  106. Have transiently depressed inflammatory and immune function. Have neutrophils that are not capable of efficient chemotaxis. Have a deficient complement system. Are deficient in collectins and collectin-like proteins. Are susceptible to bacterial infections.
  107. impaired or delayed inflammation is a result of
    chronic illness (DM CV disease)
Card Set
Stress inflammation immunity
test 2