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Pathology > 2.5 Chemical Mediators of inflammation > Flashcards

2.5 Chemical Mediators of inflammation Flashcards

1
Q

chemical mediators of inflammation

A

peptides,
lipids,
amines
- preformed or newly synthesized

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2
Q

where are these mediators found

A

in plasma

or cells

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3
Q

inflammatory mediators work by

A

binding receptors and many stimulate the release of other medeators

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4
Q

times life of inflammatory mediators

A

short lived

eg arachadonic acid

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5
Q

harmful to body

A

potentially - don’t have inflammation until you make the mediators so you only have it where you want it but some like IL1 and TNF float around causing systemic effects

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6
Q

vasoactive amines

A

small molecular weight amines

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7
Q

vasoactive amines are found in

A

mast cells and platelets

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8
Q

vasoactive amines: preformed or synthesized

A

preformed and sequestered in cellular granules (active, not zymogens) ex histamine

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9
Q

Histamine found mostly in

A

mast cells

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10
Q

histamine is released by

A

physical injury,
IgE,
C3a and C5a,
cytokines (IL1 IL8)

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11
Q

fn of histamine

A

constricts large arteries,
vasodialation (small art)
and increased vascular permeability (venous)

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12
Q

histamine causes

A

itching pain

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13
Q

histamine works by

A

binding to H1 receptors

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14
Q

serotonin is found in

A

platelets but NOT mast cells

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15
Q

serotonin actions

A

same as histamine

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16
Q

role in inflammatory response of serotonin

A

in rats it is found in mast cells but we don’t know its role in human inflammation. Mostly described in the CNS

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17
Q

complemet

A

proteases found in plasma that are preformed as zymogens

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18
Q

complement activation (cascade) paths

A

classical,
alternative,
lectin

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19
Q

classical complement

A

ag-aby complex–>C1qrs complex
that cleaves C2 and C4 liberating C4a and
froming C3 convertase,

C3 convertase cleaves C3 liberating C2a and C3 b,

C3b associates with C3 convertase and activates C5 liberating C5a,

activated C56789 forms the MAC

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20
Q

C3a C4a and C5a are

A

chemotactic, but mostly C5a

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21
Q

C3b is an

A

opsonin

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22
Q

alternative path

A

microbial surfaces –> C3 –> C3a and C3b,

C3b –> C5 –> C5a + C5b(–>MAC)

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23
Q

Lectin path

A

plasma lectin binds to microbe C2, C4 act - C3a and 5a are liberated _slide 99

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24
Q

C3a and C5a are

A

anaphylatoxins –> C4a too a little

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25
Q

C5b and C6, 7, 8, 9

A

MAC complex

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26
Q

C3a

A

histamine release from mast cells (vasodialation and inc. vascular permeability indirectly)

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27
Q

C5a

A 
histamine release from mast cell, 
AA metabolism, 
leukocyte chemotaxis, 
adhesion, 
activation
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28
Q

Plasmogen activator –> plasminogen –> plasmin

A

plasmin truns fibrin into split products, and

cleaves C3 and C5 to relieve C3a and C5a

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29
Q

central and commited step of complement

A

formation fo C3a and C3b - this step is the focus of regulatin

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30
Q

DAF

A

decay accelerating factor
enhances disassociation of C3 convertase
(to inhibit further activation of complement)

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31
Q

factor 1

A

proteolytically cleaves C3b

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32
Q

C1 inhibitor

A

binds C1 to inhibit it

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33
Q

CD59

A

inhibits final assembly of MAC

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34
Q

C3 deficiency

A

death from infections if not treated

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35
Q

C2 and C4 deficiency

A

get autoimmune diseases especially lupus

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36
Q

MAC deficiencies

A

get Neisseria infections

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37
Q

defect in linking protein linking DAF and VD 59 to RBC

A

paroxysmal nocturnal hemoglobinuria–>red cells can’t defend themselves_.
red cells normally have this linking protein binding this inhibitors of complement so activated complement doesn_t destroy your red cells

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38
Q

T cell deficiencies

A

really strange opportunistic infections

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39
Q

Kinin System

A

Peptieds in the plasma as zymogens

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40
Q

factor 12 involved in

A

the clotting cascade and prekallikrein (protein in plasma) pathway

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41
Q

factor 12a –> prekallikrein path

A

prekallikrein –> Kallikrein –> high MW Kiniogin –> Bradykinin

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42
Q

Kallikrein

A

involved in factor 12 regeneration, C5 cleavage to C5a, conversion to Plasmin (by plasminogen)

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43
Q

Bradykinin

A

peptide that acts like histamine

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44
Q

Bradykinin causes

A

inc vascular permeability, vasodilatation of small vessels, pain, contraction of large vessels

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45
Q

Coagulation system

A

factor 12, thrombin, fibrinopeptides generated, factor 10a

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46
Q

factor 12

A

kinin system

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47
Q

thrombin

A

binds protease activated receptors (PARs) on many cells stimulating many inflammatory reactions - if you’re making thrombin you’re not well so it makes sense to have crosstalk with inflammation, commited step of coagulation cascade

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48
Q

Factor 10a (Xa)

A

directly inflammatory

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49
Q

Fibrinolytic System

A

plasminogen –> plasminogen –> Plasmin

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50
Q

Plasmin involved in

A

C3/5 cleavage, Fibrin split product formation, factor 12a formation

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51
Q

activated factor 12(12a) / (XII) activates

A

kinins, thrombin, plasmin split products, C3a/5a formation via plasmin

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52
Q

C3a and 5a are fromed from

A

classic pathway, alternative pathway, microbes, plasmin

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53
Q

arachidonic acid metabolites

A

lipid in cells that are synthesized

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54
Q

Arachidonic acid is a

A

20 carbon unsaturated fatty acid (5 8 11 14 cicosatetraenoic acid)

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55
Q

AA is derived fomr

A

dietary sources or synthesized form linoleic acid

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56
Q

In phospholipids AA is

A

esterified especially at the 2 carbon position of phosphatidyl-choline, inositol and ethanolamine

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57
Q

different cells will have particular enzymes to creat AA metabolites such as

A

cyclooxygenases (prostaglandins),

lipooxygenases (leukotrienes)

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58
Q

Phospholipases turn

A

phospholipids into AA

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59
Q

Steroids will inhibit

A

first commited stip shutting down AA synthesis and all its metabolites by extension

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60
Q

asprin and NSAIDS

A

only stop cyclooxygenases

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61
Q

how do we inhibit the synthesis of lipoxygenases

A

can only stop it from by steroids earlier in the path, preventing AA from forming

62
Q

cyclooxygenases

A

COX1 and COX2

63
Q

COX1/2 –>

A

PGG2 –> PGH2

64
Q

PGH2 –>

A 
PGI2 (prostacyclin), 
TXA2, 
PGD2, 
PGE2, 
PGF2alfpha
65
Q

vasodialation

A

PG I2, E2, D2

66
Q

inc vascular permeability

A

PGD2

67
Q

vasoconstriction

A

TXA2

68
Q

pain

A

PGE2

69
Q

platelet aggregation

A

TXA2

70
Q

inhibition of platelet aggregation

A

PGI2

71
Q

fever

A

PGE2, fever enhances the actions of other mediators

72
Q

TXA2 syn in

A

platelets

73
Q

PGI2 syn in

A

endothelial cells

74
Q

PGD2 syn in

A

mast cells

75
Q

5HETE, LTB4 syn in

A

neutrophils and some macrophages

76
Q

LTC4 LTD4 LTE4 syn in

A

mast cells

77
Q

Lipoxins syn in

A

platelets (must cooperate with other cells to get LTA4)

78
Q

lipoxygenases path starts with

A

5LO –> 5-PHETE

79
Q

5PHETE –>

A

5HETE and LTA4

80
Q

LTA4 –>

A

LTB4,C4, D4,E4, and lipoxin

81
Q

LTA4 –>LTC4 via

A

adding glutathione

82
Q

LTA4 –>LTD4 via

A

losing one aminoacid

83
Q

LTA4 –>LTE4 via

A

losing one aminoacid

84
Q

LTA4 –>lipoxins via

A

12-lipoxygenase in platelets

85
Q

LTB4 is chemotactic fo

A

nformyl peptides

86
Q

LT C D and E are

A

cystenyl leukotryines

87
Q

LT C D and E actions

A

vasoconstriction,
bronchoconstriction,
inc vasc permeability

88
Q

LTB4, lipoxins, and 5HETE actions

A

chemotaxis,

leukocyte adhesion

89
Q

lipoxins are required for

A

cell-cell contact

90
Q

lipoxins are made from

A

LTA4 generated in other cells

91
Q

lipoxins inhibit

A

vasoconstircion induced by LTC4,

neutrophil chemotaxis and adhsion

92
Q

Lipoxins stimulate

A

vasodialation,

monocyte activities –> seen in switch from acute to chronic

93
Q

Lipoxins vs leukotrienes relationship

A

inverse

94
Q

Asprin and NSAIDs inhibit

A

COX1 and COX2

95
Q

Celebrex inhibits

A

COX2 and later COX1 _.remeber fda study comparing celebrex and asprin

96
Q

Zileuton inhibits

A

5LO

97
Q

receptor antagonists for cysteinyl leukotrienes

A

montelukast (singulari) Zafirlukast, Pranlukast

98
Q

glucocorticosteroids inhibit

A

phospholipases and downregulate COX2

99
Q

Where is cox1 made

A

in the stomach - needed to protect against stomach acid

100
Q

How does asprin work

A

acetylsiacilic acid causes irreversible shut down by acethylating cyclooxygenase

101
Q

asprin also inhibits synthesis of

A

prostacyclin

102
Q

give low dose asprin to

A

turn off platelets and prevent coagulation

103
Q

fish oils

A

have less arachidonic acid and proinflammtory processes aer less

104
Q

PAF - platelet activating factor

A

is made of lipd found in cells and are synthesized

105
Q

PAF is a bioactive lipid called

A

acetyl-glyceryl-ether phosphorylcholine - glycerol backbone with long chain fatty acid in A position, short chain in B position and PC in C.
original long FA in B removed by phospholipase A2 then acetylated by acetyltransferase

106
Q

PAF is found in

A

all infammatory cells and endothelial cells

107
Q

PAF at high concentrations causes

A

constriction—an invitro arteaffect?

108
Q

PAF at low concentrations causes

A

dialation, 10000 more potent than histamine

109
Q

PAF induces

A 
platelet aggregation, 
leukocyte adhesion, 
and chemotaxis, 
degranulation, 
and oxidative burst
110
Q

PAF binds

A

a single G-protein coupled receptor

111
Q

PAF in the oxididzed forms is found in

A

cigarette smokers that enhance platelet,
leukocyte,
and endothelial interactions

112
Q

cytokines and chemokines

A

are proteins/peptides in cells that are both preformed and synthesized but usually synthesized

113
Q

Interleukins

A

IL1, IL2 etc

114
Q

Interferons

A

Type I alpha and beta, type 2 gamma

115
Q

colony stimulating factors

A

GM-CSF, MCSF, GCSF

116
Q

TNF

A

alpha and beta

117
Q

TGF

A

beta

118
Q

inflammatory cytokines

A

IL1 and TNFalpha and beta

119
Q

IL1 and TNF are secreted by

A

macrophages

120
Q

TNF beta is secreted by

A

T cells

121
Q

IL1 is secreted by

A

many other cells

122
Q

TNF and IL1 both can have

A

autocrine,
paracrine or
endocrine effects

123
Q

TNF and IL1 mainly act on

A

leukocytes,
endothelium,
fibroblasts, and
systemic acute phase reactions

124
Q

Endothelium can

A 
inc syn of adhesion molecules, 
inc PGI synthesis, 
inc procoagulant activity, 
dec anticoagulant activity, 
inc IL1 secretion
125
Q

leukocytes can

A

prime for enhanced activity,
inc cytokine secretion (TNF, IL1, IL2_IL6, IL8, PDGF),
inc affinity of adhesion molecules

126
Q

fibroblasts cause

A

inc proliferation,
inc collagen synthesis,
inc collagenase and protease activity,
inc PGE2 secretion

127
Q

in some fibrotic diseases scaring comes from

A

unregulated cytokine secretion

128
Q

Systemic acute phase response

A

vasodialation, fever, dec appetite, inc sleep, acute phase proteins, neutrophilia

129
Q

vasodialation can cause

A

shock

130
Q

fever interacts with

A

PGE2

131
Q

acute phase proteins are

A 
C reactive protein, 
SAA, 
SAP, 
C', 
coagulants
132
Q

TGF beta and IL10 are made by

A

many cell types including macrophages

133
Q

TGF beta and IL10 have different effects

A

on different cells

134
Q

TGF beta and IL10 are

A

antiinflammatory

135
Q

TGF beta and IL10 stimulate

A

fibroblasts and healing reactions

136
Q

Chemokines

A

chemokines are acctivators or attractants to specific types of leukocytes

137
Q

fours subtypes pased on arangement of cysteins

A

CXC, C, CX3C, CC

138
Q

CXC

A

one AA separating cysteins,

act on neutrophils (IL8)

139
Q

C-C

A

act on macorphages and monocytes (MCP1)

140
Q

C act on

A

lymphoctyes

141
Q

CX3C

A

on long stalk,
soluble and
cell bound endothelial cells.
Binds or attracts t-cell and monocytes

142
Q

Nitric oxide

A

a soluble gas in cells that is synthesized

143
Q

NO synthetase

A

constitutive or inducible found in
endothelial cells,
macrophages, and
neurons

144
Q

3 forms of NO

A

eNOS,
nNOS,
iNOS

145
Q

rezction of NO

A

arginine + o2 —-> NO + citruline

146
Q

effects of NO

A

paracrine - generation of GMP,
vasodialation (shock),
antimicrobial,
with ROS yeilds peroxynitrite and other damaging compunds

147
Q

vasodialation mediators

A

prostaglandins,

NO

148
Q

inc vasc permeability

A 
vasoactive amines, 
C3a and C5a, 
bradykinin, 
leukotrienes C4 D4 E4, 
PAF, 
Substance P
149
Q

Chemotaxis and leukocyte activation

A

C5a,
LTB4,
Chemokines,
Bacterial products

150
Q

Fever

A

IL1
IL6
TNF

151
Q

Pain

A

prostaglandins,

bradykinin

152
Q

Tissue damage

A

neutrophils and macrophages lysosomal enzymes,
oxygen metabolites,
nitric oxide

Pathology (26 decks)

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