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Pathology I > 7: acute inflammation II > Flashcards

7: acute inflammation II Flashcards

1
Q

what is the function of opsonins

A

recognition and attachment for phagocytosis

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2
Q

antibody
complement C3b
mannose-binding lectin

A

opsonins

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3
Q

oxygen dependent killing of organisms

A

1) oxygen is reduced to superoxide via NADPH oxidase
2) superoxide is converted to H2O2 by superoxide dismutase
3) myeloperoxidase from PMN granules catalyzes rxn between Cl and H2O2 forming hypochlorus acid

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4
Q

what is hypochlorus acid

A

a powerful oxidant and antimicrobial

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5
Q

what are some oxygen independent killing pathways

A

leukocyte granule proteins and enzymes (acid hydrolases, lysozyme, lactoferrin, cationic proteins)

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6
Q

what are the 4 things an activated leukocyte can do?

A
  • produce arachidonic acid metabolites
  • degranulate and secrete lysosomal enzymes/ oxidative burst
  • secrete cytokines
  • modulate leukocyte adhesion molecules
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7
Q

where do mediators of inflammation originate from?

A

plasma (precursor form) or cells (sequestered in granules or synthesized)

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8
Q

what are the effects of histamine and serotonin

A
  • immediate but transient (1 hr)
  • arteriolar dilation
  • increased permeability of postcapillary venules
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9
Q

what is the effect of histamine and serotonin on large arteries

A

constriction

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10
Q

what cytokines stimulate release of vasoactive amines from mast cells?

A

IL-1 and IL-8

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11
Q

critical step of complement activation

A

cleavage of C3

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12
Q

classic pathwya of complement activation

A

binding of an antigen-antibody complex to C1

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13
Q

alternate pathway of complement activation

A

C3 directly activated by bacterial endotoxins, complyx polysaccs, or aggregated immunoglobulins

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14
Q

lectin pathway of complement activation

A

C1 activation by binding of mannose-binding lectin to carbs on microbes

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15
Q

C3a, C4a, C5a —?

A

stimualte histamine release from mast cells = increased vascular permeability and vasodilation

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16
Q

C5a–?

A
  • chemotaxis of monocytes and granulocytes
  • increase surface expresseion of leukocyte CAM
  • activates lipoxygenase pathway in PMNs and monocytes
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17
Q

C3b —-?

A

opsonization with recognition by receptors on PMNs, macrophages and eosinophils

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18
Q

C5-9 —-?

A

membrane attack complex that inserts into lipid bilayer forming macropores that increase cell permeability and lead to lysis

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19
Q

factor XII of the intrinsic clotting system

A

hagemnan factor

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20
Q

what activates hageman factor

A

direct contact with endotoxins, collage or basement membrane

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21
Q

what does an activated hageman factor triggers what systems (2)?

A

kinin system and clotting cascade

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22
Q

activated hageman factor converts prekallikrein into _______________ which…

A

kallikrein

  • amplifies activation of hageman fator
  • cleaves kininogen to form kinins
  • converts plasminogen to plasmin
  • is chemoattractant for PMNs and converts C5 to C5a to attract WBCs
  • increases CAM expression on endothelium
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23
Q

what effects does bradykinin have?

A
  • increases vascular permeability
  • dilates blood vessels
  • contracts non-vascular smooth muscle
  • causes pain
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24
Q

what inactivates bradykinin

A

plasma kininase

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25
cascade of rxns resulting in fibrin clot which is then dissolved by the fibrinolytic system
coagulation-fibrinolytic system
26
protease that cleaves circulating soluble fibrinogen to generate insoluble fibrin
thrombin
27
lyses fibrin clots
plasmin
28
how is plasmin formed?
cleaving of plasminogen by kallikrein or plasminogen activator released by endothelium and leukocytes
29
what are the actions of plasmin in inflammation
- activates hageman factor - cleaves C3 to C3a - degrades fibrin to form fibrin split products ( increase vascular permeability)
30
normally bound to cell membrane phospholipids and is released by the action of cellular phospholipases by mechanical, chemical and physical stimuli including C5a
arachidonic acid
31
inhbit cyclooxygenase preventing formation of the whole family
aspirin and NSAIDs
32
act indirectly by inhibiting phospholipasese
glucocorticoids
33
COX converts ________ into ___________
arachidonic acid into prostaglandin intermediates Cocks? keep it PG, ay?
34
what prostoglandin intermediates are produced by COX?
``` thromboxane A2 PGI2 PGE2 PGD2 PGF2a PGE2 ```
35
potent platelet aggregator and vasoconstrictor
TXA2
36
vasodilatior and ihbitor of platelet aggregation
PGI2
37
sensitizes skin to painful stimuli and plays role in cytokine-induced fever
PGE2
38
PG intermediates which cause vasodilation and potentiate edema
PGD2 PGF2a PGE2
39
how does aspirin stop vasoconstriction and platelet aggregation
inhibits production of TXA2
40
coverts arachidonic acid inot leukotrienes and lipoxins
lipoxygenase pathway LOX
41
potent chemoattractant causing PMN aggregation and adhesion to endothelial cells, generation of ROS and release of lysosome
LT B4
42
LT C4, D4, E4 ---->
cause intense vasoconstriction and bronchospasm and increase vascular permeability
43
endogenous negative regulators of leukotriene action
lipoxins
44
principal actions of lipoxins
inhibit leukocyte recruitment and the cellular activites of inflammation
45
Lipoxin A4 and B4 --->
inhibit PMN adhesion ot endothelium and PMN chemotaxis
46
COX inhibitors, aspirin and indomethacin inhibit
cyclooxygenase
47
steroids inhibit...
phospholipases that produce arachidonic acid
48
causes platelet aggregation and release of platelet products
platelet activating factor
49
PAF at higher concentrations causes...
vasoconstriction and bronchoconstriction
50
PAF at lower concentration cuases...
vasodilation and venular permeability
51
polypeptides with strong chemotactic properties
chemokines
52
key cytokines of inflammation
interleukin-1 IL-1 and Tumor Necrosis Factro TNF
53
what is the main producer of IL-1 and TNF
activated macrophages
54
produce fever, affect sleep and appetitie, produce acute-phase proteins; cause neutrophilia and hemodynamic effects in shock
acute phase cytokine reactions
55
endothelial effects of TNF and IL-1
increase leukocyte adherence, stimulate PGI synthesis, increase procoagulant activity, and increase production of IL1, 6, 8, and PDGF
56
fibroblast effects of TNF and IL-1
increase proliferation, collagen synthesis, and PGE synthesis and increase protease and collagnease production
57
leukocyte effects of TNF and IL-1
increase cytokine secretion (IL-1 and IL-6)
58
local fibroblast effects of TNF/IL1
increased proliferation and increased collagen synthesis
59
local leukocyte effects of TNF/IL1
activation and production of cytokines
60
local vascular endothelium effects of TNF/IL1
increased -expression of leukocyte adhesion molecules - production of Il-1, chemokines - increased procoagulant activity and decreased anticoagulant activity
61
systemic effects of TNF and IL-1
- fever - leukocytosis - increase acute pase proteins - decrease appetitie - increase sleep
62
how are chemokines classified
according to cysteine residues in the protein
63
CXC/alpha
act on neutrophils
64
what type of chemokine is IL-8
CXC/alpha
65
C-C/beta chemokines
attract NOT nuetrophils
66
what type of chemokine is eotaxin
c-c/ beta
67
chemokines specific for lymphocytes
C or gamma
68
CX3C
fractalkine is strong attractant for monocytes and T-cells
69
acts in paracrine fashion on target cells through cGMP
nitric ocide
70
strong vasodilation through smooth muscle cell relaxation
nitric oxide also reduces platelt aggregation and adhesion and WBC recruitment; microbicidal
71
ROS release extracellulary cause
- endothelial cell damage - inactivation of antiproteases - injury to other cells
72
the 2 neuropeptides
substance P and neurokinin A
73
biological functions substance P
- transmission of pain signals - regulation of blood pressure - increase vascular permeability

Pathology I (12 decks)

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