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MFMII > Inflammatory Mediators > Flashcards

Inflammatory Mediators Flashcards

1
Q

effect of histamine release

A

dilation of arterioles and increased permeability of venules by producing interendothelial gaps due to retraction of endothelial cell

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2
Q

how is histamine mediated?

A

binding to H1 receptors on microvascular endothelial cells

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3
Q

what does production of histamine induce

A

induces synthesis of prostacyclin and nitric oxide (smooth muscle relaxants and vasodilation)

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4
Q

what are things that stimulate release of histamine from mast cells

A

trauma, cold, heat, binding of Ab to mast cell, C3a and C5a, IL-1, IL-8, substance P, histamine releasing proteins from WBC

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5
Q

where are histamines stored

A

preformed and stored in granules and released immediately

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6
Q

what is the source of serotonin?

A

platelets and some neuroendocrine cells

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7
Q

when is serotonin released?

A

released with histamine during platelet aggregation

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8
Q

what does serotonin do

A

vasoconstrictor and is a neurotransmitter in the GI tract

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9
Q

what do steroids do

A

inhibits phospholiases that are needed for the arachidonic acid pathway. reduce transcription of genes encoding COX-2, phospholipase A2, proinflammatory cytokines and iNOS

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10
Q

what is produced in the arachidonic acid pathway

A
  1. cylooxygenases

2. 5-lipooxygenase

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11
Q

what does prostacyclin do (PGI2)

A

vasodilation, inhibit platelet aggregation

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12
Q

what does thromboxane A2 do?

A

vasoconstriction, promote platelet aggregation

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13
Q

what does PGE/PGD do

A

vasodilation, increased vascular permeability

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14
Q

what pathway makes prostaglandins and thromboxanes?

A

cyclooxygenase (COX)

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15
Q

what do aspirin, indomethacin do?

A

inhibit COX1 and COX2 (inhibit making of prostaglandins and thromboxanes)

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16
Q

how is leukotriene B4 made?

A

5-lipooxygenase makes 5-HETE which makes leukotriene B4

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17
Q

what makes leukotriene C4, D4, and E4

A

5-lipooxygenase

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18
Q

what do leukotrienes C4, D4, and E4 do

A

bronchospasm and increased vascular permeability

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19
Q

what does PGE2 do?

A

pain and fever

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20
Q

what are the main causes of pain in inflammation

A

PGE2 and bradykinin

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21
Q

what are ecosinoids

A

arachidonic acid metabolites (lipid products)

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22
Q

how are ecosinoids made

A

membrane amino acids are rapidly converted by enzymes into prostaglandins and leukotrienes when cells are activated by diverse stimuli

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23
Q

what do phosphoplipases do

A

release membrane amino acids into cell cytoplasm to be metabolized by 1 of 2 enzymatic pathways

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24
Q

what do steroids do

A

inhibit phospholipases that release membrane AA into cell cytoplasm to enter lipooxygenase or cyclooxygenase pathways

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25
Q

what does the cyclooxygenase pathway produce?

A

prostaglandins and thromboxane

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26
Q

what does the lipooxygenase pathway produce?

A

leukotrienes and lipoxins

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27
Q

what do PGD2, PGE2, PGF2 do

A
  1. vasodilation

2. potentiate edema by enhancing vascular permeability effects of other mediators

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28
Q

what does PGE2 do specifically

A

mediates pain and is involved in cytokine induced fever with infections

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29
Q

what does PGI2 do? prostacyclin

A

is released from endothelium and vasodilates and inhibits platelet aggregation

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30
Q

what does thromboxane A2 do

A

released from platelets and vasoconstricts and promotes platelet aggregation

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31
Q

cyclooxygenase pathway products

A
  1. PGI2 prostacyclin
  2. thromboxane A2
  3. PGD2, PGE2, PGF2
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32
Q

lipooxygenase pathway products

A
  1. leukotriene B4 (LTB4)
  2. leukotriene C4, D4, E4
  3. lipoxins A4 and B4
33
Q

what does leukotriene B4 do

A

neutrophil chemotaxis

34
Q

what does leukotriene C4, D4, and E4 do

A

increase vascular permeability by endothelial cell contraction, vasoconstriction, bronchospasm

35
Q

what do lipoxins A4 and B4 do

A

inhibitors of inflammation

36
Q

what 2 cells are required for lipoxin synthesis

A
  1. leukocytes (neutrophils) produce intermediates in lipoxin synthesis
  2. platelets convert these intermediates to lipoxins
37
Q

what do lipoxins actually do

A

inhibit neutrophil adhesion and chemotaxis, play role in resolution of inflammation

38
Q

what eicosanoids do vasodilation

A

prostaglandins PGI2 (prostacyclin), PGE1, PGE2, PGD2

39
Q

what eicosanoids do vasoconstriction

A

thromboxane A2 and leukotrienes C4, D4, E4

40
Q

what eicosanoids do increased vascular permeability

A

leukotrienes C4, D4, E4

41
Q

what eicosanoids do chemotaxis and leukocyte adhesion

A

leukotrienes B4 and HETE

42
Q

what eicosanoid causes bronchospasm?

A

leukotrienes C4, D4, E4

43
Q

what do cytokines do

A

mediate and regulate immune and inflammatory reactions

44
Q

what cells make cytokines

A

activated leukocytes, endothelial epithelial cells, and connective tissue cells

45
Q

what do IL-1 and TNF do

A
  1. endothelial activation
  2. activation of leukocytes and other cells
  3. systemic acute phase response
46
Q

what is the systemic acute phase response

A

fever, cachexia (TNF), and sepsis syndrome

47
Q

how does IL-1 and TNF help with endothelial activation

A

increased adhesion molecules, increased procoagulant activity, increased mediators like cytokines, chemokines, GF, eicosanoids

48
Q

what is the critical step in complement activation

A

proteolysis of C3 by one of 3 different pathways (classical, alternative, lectin)

49
Q

what do the complement pathways lead to

A

formation of C3 convertase which splits C3 into C3a and C3b

50
Q

what forms the membrane attach complex

51
Q

what is C3b

52
Q

what is C3a and C5a

A

anaphylatoxins, stimulate release of histamine

53
Q

what is C5a

A

leukocyte chemotactic factor

54
Q

what are the important regulatory proteins of complement

A
  1. C1 inhibitor
  2. delay accelerating factor (DAF)
  3. CD59
55
Q

what does CD59 do

A

inhibits formation of membrane attack complex

56
Q

what is deficient in paroxysmal nocturnal hemoglobinuria

A

CD55 and CD59 are deficient on red cells, red cells prone to lysis

57
Q

what does DAF do

A

is CD55

prevents formation of C3 convertase

58
Q

what does C1 inhibitor do

A

block activation of C1

59
Q

what causes hereditary angioedema

A

inherited deficiency of C1 inhibitor

60
Q

what does platelet activating factor do

A
  1. vasoconstriction, bronchoconstriction
  2. increased leukocyte adhesion to endothelium, chemotaxis, degranulation, oxidative burst
  3. boost synthesis of other mediators esp eicosanoids
61
Q

what does PAF do in low concentration

A

causes vasodilation and increased venular permeability with a greater potency than histamine

62
Q

what cells make PAF

A

platelets, basophils, mast cells, neutrophils, macrophages, endothelial cells

63
Q

when does clotting cascade occur

A

clotting and inflammation occur together

tissue injury that leads to clotting will lead to inflammation.

64
Q

what is kinin

A

vasoactive peptides derived from plasma proteins called kininogens

65
Q

what converts kininogen to kinin

A

killikrein protease

66
Q

what does killikrein do

A

cleaves high molecular weight kininogen (HMWK) into bradykinin

67
Q

what activates kinin cascade

A

activated factor XII in the clotting system (hageman factor)

68
Q

effects of bradykinin

A
  1. vasodilation and increased vascular permeability
  2. major contributor to pain that accompanies inflammation
  3. bronchoconstriction
69
Q

what secretes neuropeptides

A

sensory nerves and some WBC

70
Q

what neuropeptides are secreted in the peripheral and central nervous system

A

substance P and neurokinin A

71
Q

where is substance P prominent

A

GI and lungs

72
Q

what does substance P do

A

transmits pain signals, regulate BP, stimulate endocrine gland hormone secretion, increase vascular permeability

73
Q

what substance may help initiate and regulate inflammation

A

neuropeptides

74
Q

what major mediators are responsible for vasodilation?

A
  1. prostaglandins
  2. histamine
  3. kinins
  4. PAF
75
Q

what major mediators cause increased vascular permeability?

A
  1. leukotrienes
  2. histamine
  3. kinins
  4. PAF
76
Q

what major mediators cause fever?

A
  1. IL-1
  2. TNF
  3. prostaglandins
  4. systemic cytokines
77
Q

what major mediators cause pain?

A
  1. bradykinin

2. PGE2/prostaglandins

78
Q

what major mediators cause tissue damage?

A
  1. PAF
  2. complement (C5a, C3a)
  3. granulocytes
  4. cytokines
79
Q

what major mediators cause chemotaxis

A
  1. C5a
  2. interleukins
  3. TNF
  4. leukotrieneB4
  5. HETE
  6. cytokines

MFMII (29 decks)

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