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Inflammation I Flashcards

1
Q

what are the principal mediators of vasodilation

A
  1. histamine

2. prostaglandins

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2
Q

what are the principal mediators of increased vascular permeability

A
  1. histamine and serotonin
  2. C3a and C5a (liberate vasoactive amines from mast cells)
  3. leukotrienes C4, D4, E4
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3
Q

what are the principal mediators of chemotaxis, leukocyte recruitment and activation?

A
  1. TNF, IL-1
  2. chemokines
  3. C3a, C5a
  4. leukotriene B4
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4
Q

what are the principal mediators of fever?

A
  1. IL-1, TNF

2. prostaglandins

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5
Q

what are the principal mediators of pain

A
  1. prostaglandins

2. bradykinin

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6
Q

what are the principal mediators of tissue damage?

A
  1. lysosomal enzymes of leukocytes

2. ROS

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7
Q

what cells release histamine?

A
  1. mast cells
  2. basophils
  3. platelets
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8
Q

function of histamine

A

vasodilation, increased vascular permeability, endothelial activation

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9
Q

what cells release prostaglandins?

A
  1. mast cells

2. leukocytes

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10
Q

function of prostaglandins

A

vasodilation, pain, fever

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11
Q

what cells release leukotrienes?

A
  1. mast cells

2. leukocytes

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12
Q

function of leukotrienes

A

increased vascular permeability, chemotaxis, leukocyte adhesion and activation, primary for wheezing

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13
Q

what cells release cytokines like TNF, IL-1, IL-6

A
  1. macrophages
  2. endothelial cells
  3. mast cells
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14
Q

local function of cytokines

A

endothelial activation to express adhesion molecules

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15
Q

systemic function of cytokines

A

fever, metabolic abnormalities, hypotension, shock

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16
Q

what cells release PAF (platelet activating factor)

A
  1. leukocytes

2. mast cells

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17
Q

function of PAF

A

vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst

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18
Q

what cells release chemokines?

A
  1. leukocytes

2. activated macrophages

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19
Q

function of chemokines

A

chemotaxis, leukocyte activation

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20
Q

what cells release complement?

A

plasma cells in the liver

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21
Q

function of complement

A

leukocyte chemotaxis and activation, direct target killing via MAC, vasodilation via mast cell stimulation

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22
Q

what cells release kinins?

A

plasma cells in the liver

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23
Q

function of kinins?

A

increased vascular permeability, smooth muscle contraction, vasodilation, pain

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24
Q

onset of acute inflammation

A

fast: minutes or hours

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25
Q

cellular infiltrate associated with acute inflammation

A

neutrophils

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26
Q

what tissue injury or fibrosis is associated with acute inflammation?

A

usually mild and self-limited

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27
Q

what are the/ local and systemic signs of acute inflammation

A

usually prominent signs

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28
Q

onset of chronic inflammation

A

slow: days

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29
Q

cellular infiltrate associated with chronic inflammation

A

monocytes/macrophages/lymphocytes

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30
Q

what tissue injury or fibrosis is associated with chronic inflammation

A

severe and progressive injury/fibrosis

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31
Q

what are the local and systemic signs of chronic inflammation

A

less prominent signs

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32
Q

common causes of acute inflammation

A
  1. infections
  2. tissue necrosis from ischemia, trauma, physical/chemical injury
  3. foreign bodies
  4. immune or hypersensitivity reactions
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33
Q

what is the first step of inflammatory reaction

A

recognition of microbes and damaged cells

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34
Q

what are cellular mechanisms of recognition

A
  1. TLR
  2. cytosol receptors that recognize molecules that are released with cell damage
  3. circulating proteins (complement)
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35
Q

what is the sequence of events in an inflammatory reaction?

A

macrophages and other cells in tissues recognize microbes and damaged cells. this liberates mediators that trigger vascular and cellular reactions of inflammation

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36
Q

cardinal 5 signs of inflammation

A
  1. redness
  2. swelling
  3. heat
  4. pain
  5. loss of function
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37
Q

3 major local manifestations of acute inflammation

A
  1. vascular dilation and increased blood flow (erythema and warmth)
  2. extravasation and extravascular deposition of plasma fluid and proteins (edema)
  3. leukocyte emigration and acumulation in the site of injury
38
Q

what are the vascular changes in acute inflammation

A
  1. vasodilation
  2. increased permeability
  3. stasis of blood flow
  4. neutrophils marginate and adhere to endothelium and then migrate through vessel into the interstitium
39
Q

describe the vasodilation that occurs with acute inflammation

A

transient constriction of arterioles may occur first, then dilation of arterioles and opening of capillary beds (retraction of endothelia due to histamine)

40
Q

describe the impact of increased microvascular permeability

A

excess of interstitial fluid or cavity fluid (edema)

41
Q

describe why vascular congestion occurs

A

loss of fluid into the intersitium and the increased diameter of the blood vessel leads to increased concentration of RBC in the vessel, increased viscosity and slower blood flow

42
Q

what induces retraction of endothelial cells?

A

histamine and other mediators (

43
Q

what are the 2 principal causes of increased vascular permeability?

A
  1. retraction of endothelial cells (rapid and short lived)

2. endothelial injury (rapid and longer lived)

44
Q

what is exudate?

A

fluid leaking out of vessels that is high in protein and cellular content associated with acute inflammation and pus

45
Q

what is transudate

A

fluid leaking out of vessel is low in protein and cellular content

46
Q

what is transudate usually associated with

A
  1. low serum albumin (low osmotic pull)

2. increased hydrostatic pressure (heart failure)

47
Q

what could cause increased hydrostatic pressure

A

venous outflow obstruction (congestive heart failure)

48
Q

what could cause decreased colloid osmotic pressure

A

decreased protein synthesis due to liver disease or increased protein loss due to kidney disease

49
Q

what is lymphangitis

A

inflammation of lymphatic vessels

50
Q

what is lymphadenitis

A

inflammation of draining lymph node

51
Q

what do lymphatics drain

A

they drain increased interstitial fluid that has accumulated due to increased vascular permeability

52
Q

what cell types drain into lymph?

A

microbes, leukocytes, cellular debris

53
Q

steps of extravasation

A
  1. adhesion of leukocytes to vascular endothelium
  2. transmigration across endothelium (diapedesis)
  3. chemotaxis
  4. leukocyte activation
  5. phagocytosis
54
Q

what mediates rolling of leukocyte

A

E selectin and P selectin

55
Q

what activates integrins (ICAM) to tightly bind to rolling leukocyte

A

chemokines

56
Q

what makes a stable adhesion between leukocytes and endothelial cell

57
Q

what mediates diapedesis?

58
Q

how does leukocyte rolling start?

A

redistribution of P selectin from within the endothelial cytoplasm to the cell surface induced by histamine and thrombin

59
Q

what induces redistribution of P selectin

A

histamine and thrombin

60
Q

what acitvates P selectin?

A

cytokines, histamines, thrombin

61
Q

order of induction of rolling

A
  1. redistribution of adhesion molecule P selectin
  2. induction of adhesion molecule synthesis of E selectin and ligands for ICAM/VCAM
  3. increase in binding affinity of leukocyte integrins
62
Q

when does induction of adhesion molecule synthesis occur?

A

2-3 hours after induction

63
Q

what induces adhesion molecule synthesis of E electin and ICAM/VCAM?

64
Q

what increases binding affinity of leukocyte integrins?

A

chemokines

65
Q

how do leukocytes migrate through endothelium?

A

leukocyte squeezes through endothelial gaps assisted by PECAM-1/CD31

66
Q

how do leukocytes pierce the basement membrane?

A

secrete collagenases

67
Q

what cells primarily transmigrate during acute inflammation

A

neutrophils

68
Q

how does chemotaxis work

A

leukocytes move within tissue along increasing chemoattractant gradient toward site of injury

69
Q

what are important exogenous chemotactic factors for neutrophils?

A

factors originating from source of inflammation like bacterial products like peptides with N formyl methionine terminal amino acid and lipids

70
Q

what are endogenous chemotactic factors for neutrophils?

A

factors produced by the injured host

71
Q

what are the important endogenous chemotactic factors?

A
  1. complement (C5a)
  2. leukotriene B4 (LTB4)
  3. chemokines (IL-8)
72
Q

how do chemoattractants induce leukocyte movement?

A
  1. chemoattractant binds to specific receptor on leukocyte membrane
  2. binding activates intracellular phospholipase C
  3. phospholipase C causes increase in intracellular Ca within leukocyte
  4. intracellular Ca triggers crosslinking of actin within focal area of leukocyte cytoskeleton
  5. crosslinking makes a pseudopod form in the direction of the increasing density gradient of chemoattractant
73
Q

how are leukocytes activated

A
  1. recognition of offending agents which deliver signals that
  2. activate the leukocytes to ingest and destroy the offending agents and
  3. amplify inflammatory reaction
74
Q

stimulation of leukocyte produces what responses? (4)

A
  1. amplification of inflammatory reaction
  2. degranulation and release of lysosomal enzymes
  3. phagocytosis and activation of oxidative burst within leukocyte
  4. increase in binding affinity of adhesion molecules
75
Q

how do leukocytes amplify inflammatory reaction?

A
  1. production of arachidonic acid metabolites by leukocyte

2. secretion of cytokines by leukocyte

76
Q

what is superoxide dismutase

A

makes ROS into hydrogen peroxide and water

77
Q

how does extracellular release damage the host?

A
  1. damage to endothelial cells causes increased vascular permeability
  2. inactivation of antiproteases (like alpha 1 antitrypsin)
78
Q

how does alpha 1 antitrypsin damage tissue

A

inactivation of alpha 1 antitrypsin leads to unopposed protease activity with increased tissue destruction

79
Q

what is catalase

A

detoxifies hydrogen peroxide

80
Q

what is ceruloplasmin

A

copper containing serum protein (carries copper)

81
Q

what are the antioxidant mechanisms

A
  1. superoxide dismutase
  2. catalase
    3 ceruloplasmin
  3. iron free fraction of serum transferrin
82
Q

what produces NO?

A

endothelial cells and macrophages

83
Q

action of NO

A
  1. potent vasodilator

2. kills microorganisms

84
Q

how does NO kill microorganisms

A

interacts with oxygen derived free radicals to produce antimicrobial substances which can kill microorganisms within macrophage phagolysosomes

85
Q

what are neutrophils primary/azurophillic granules

A
  1. myeloperoxidase (MPO)
  2. bactericidal factors (lysozyme, defensins)
  3. acid hydrolases
  4. neutral proteases (elastase, collagenases, proteinases)
86
Q

what are neutrophil’s secondary/specific granules

A
  1. lysozyme
  2. collagenase
  3. gelatinase
  4. lactoferrin
  5. plasminogen activator
  6. histaminase
  7. alkaline phosphatase
87
Q

what are monocytes/macrophages lysosomal constituents?

A
  1. acid hydrolase
  2. collagenase
  3. elastase
  4. phospholipase
  5. plasminogen activator
88
Q

what holds extracellular release of lysosomal enzymes in check?

A

antiproteases like alpha-1-antitrypsin and alpha2 macroglobulin

89
Q

what are NETS

A

fibrillary networks containing antimicrobial substances produced by neutrophils

90
Q

what do NETS fibrillary network consist of?

A
  1. nuclear chromatin

2. contents of cytoplasmic granules (antimicrobial proteins and enzymes)

91
Q

where are inflammatory mediators derived?

A

cells or plasma proteins in response to various stimuli like substances from microbes and necrotic cells, complement and other proteins

MFMII (29 decks)

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