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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
Q

cascade of rxns resulting in fibrin clot which is then dissolved by the fibrinolytic system

A

coagulation-fibrinolytic system

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26
Q

protease that cleaves circulating soluble fibrinogen to generate insoluble fibrin

A

thrombin

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27
Q

lyses fibrin clots

A

plasmin

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28
Q

how is plasmin formed?

A

cleaving of plasminogen by kallikrein or plasminogen activator released by endothelium and leukocytes

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29
Q

what are the actions of plasmin in inflammation

A
  • activates hageman factor
  • cleaves C3 to C3a
  • degrades fibrin to form fibrin split products ( increase vascular permeability)
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30
Q

normally bound to cell membrane phospholipids and is released by the action of cellular phospholipases by mechanical, chemical and physical stimuli including C5a

A

arachidonic acid

31
Q

inhbit cyclooxygenase preventing formation of the whole family

A

aspirin and NSAIDs

32
Q

act indirectly by inhibiting phospholipasese

A

glucocorticoids

33
Q

COX converts ________ into ___________

A

arachidonic acid into prostaglandin intermediates

Cocks? keep it PG, ay?

34
Q

what prostoglandin intermediates are produced by COX?

A 
thromboxane A2
PGI2
PGE2
PGD2
PGF2a
PGE2
35
Q

potent platelet aggregator and vasoconstrictor

A

TXA2

36
Q

vasodilatior and ihbitor of platelet aggregation

A

PGI2

37
Q

sensitizes skin to painful stimuli and plays role in cytokine-induced fever

A

PGE2

38
Q

PG intermediates which cause vasodilation and potentiate edema

A

PGD2
PGF2a
PGE2

39
Q

how does aspirin stop vasoconstriction and platelet aggregation

A

inhibits production of TXA2

40
Q

coverts arachidonic acid inot leukotrienes and lipoxins

A

lipoxygenase pathway LOX

41
Q

potent chemoattractant causing PMN aggregation and adhesion to endothelial cells, generation of ROS and release of lysosome

A

LT B4

42
Q

LT C4, D4, E4 —->

A

cause intense vasoconstriction and bronchospasm and increase vascular permeability

43
Q

endogenous negative regulators of leukotriene action

A

lipoxins

44
Q

principal actions of lipoxins

A

inhibit leukocyte recruitment and the cellular activites of inflammation

45
Q

Lipoxin A4 and B4 —>

A

inhibit PMN adhesion ot endothelium and PMN chemotaxis

46
Q

COX inhibitors, aspirin and indomethacin inhibit

A

cyclooxygenase

47
Q

steroids inhibit…

A

phospholipases that produce arachidonic acid

48
Q

causes platelet aggregation and release of platelet products

A

platelet activating factor

49
Q

PAF at higher concentrations causes…

A

vasoconstriction and bronchoconstriction

50
Q

PAF at lower concentration cuases…

A

vasodilation and venular permeability

51
Q

polypeptides with strong chemotactic properties

A

chemokines

52
Q

key cytokines of inflammation

A

interleukin-1 IL-1 and Tumor Necrosis Factro TNF

53
Q

what is the main producer of IL-1 and TNF

A

activated macrophages

54
Q

produce fever, affect sleep and appetitie, produce acute-phase proteins; cause neutrophilia and hemodynamic effects in shock

A

acute phase cytokine reactions

55
Q

endothelial effects of TNF and IL-1

A

increase leukocyte adherence, stimulate PGI synthesis, increase procoagulant activity, and increase production of IL1, 6, 8, and PDGF

56
Q

fibroblast effects of TNF and IL-1

A

increase proliferation, collagen synthesis, and PGE synthesis and increase protease and collagnease production

57
Q

leukocyte effects of TNF and IL-1

A

increase cytokine secretion (IL-1 and IL-6)

58
Q

local fibroblast effects of TNF/IL1

A

increased proliferation and increased collagen synthesis

59
Q

local leukocyte effects of TNF/IL1

A

activation and production of cytokines

60
Q

local vascular endothelium effects of TNF/IL1

A

increased -expression of leukocyte adhesion molecules

  • production of Il-1, chemokines
  • increased procoagulant activity and decreased anticoagulant activity
61
Q

systemic effects of TNF and IL-1

A
  • fever
  • leukocytosis
  • increase acute pase proteins
  • decrease appetitie
  • increase sleep
62
Q

how are chemokines classified

A

according to cysteine residues in the protein

63
Q

CXC/alpha

A

act on neutrophils

64
Q

what type of chemokine is IL-8

A

CXC/alpha

65
Q

C-C/beta chemokines

A

attract NOT nuetrophils

66
Q

what type of chemokine is eotaxin

A

c-c/ beta

67
Q

chemokines specific for lymphocytes

A

C or gamma

68
Q

CX3C

A

fractalkine is strong attractant for monocytes and T-cells

69
Q

acts in paracrine fashion on target cells through cGMP

A

nitric ocide

70
Q

strong vasodilation through smooth muscle cell relaxation

A

nitric oxide

also reduces platelt aggregation and adhesion and WBC recruitment;
microbicidal

71
Q

ROS release extracellulary cause

A
  • endothelial cell damage
  • inactivation of antiproteases
  • injury to other cells
72
Q

the 2 neuropeptides

A

substance P and neurokinin A

73
Q

biological functions substance P

A
  • transmission of pain signals
  • regulation of blood pressure
  • increase vascular permeability

Pathology I (12 decks)

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