Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Disease and Defense > Inflammatory Mediators > Flashcards

Inflammatory Mediators Flashcards

1
Q

Examples of Vasoactive Amines

A

Histamine, Seratonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Sources of Vasoactive Amines

A

Basophils (circulating), mast cells (tissue based), platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which inflammatory mediators are pre-formed in granules?

A

Histamine, Seratonin, lysosomal enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Sources of Histamine

A

platelets, mast cells, basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sources of Seratonin

A

platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Effects of Histamine

A

immediate/delayed; early smooth muscle contraction, increased vasculature permeability(early), mucous secretion, chemotaxis of white blood cells (Late-phase reaction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Inactivation of histamine

A

histaminase from PMNs, liver, macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

causes of histamine release

A

IgE Fc interaction (type I/immediate hypersensitivity), tissue injury, C3a/5a interactions, IL-1, IL-8 (cytokines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Release of seratonin: cause

A

platelet aggregation due to exposure to collagen, thrombin, PAF, TXA2, other substainces; released in context of platelet congregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Effects of seratonin

A

similar to histamine: increase

vasculature permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Examples of Eicosanoids

A

Prostaglandins (PG), Leukotrienes (LT), Thromboxanes (TX), Lipoxins (LX)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Precursor of Eicosanoids

A

arachidonic acid (AA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what kind of molecules are Eicosanoids?

A

lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

sources of Eicosanoids

A

white cells, platelets, endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

actions of eicosanoids

A

vasodilator (PGI2), vasoconstrictor (TXA2), Vasculature permeability (LT), chemotaxis (LT), promote Platelet aggregation (TXA2, platelets), inhibit platelet aggregation (PGI2, endothelial cells), smooth muscle effects (bronchus, uterine contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Platelet activating Factor

A

Phospholipid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Source of Platelet activating factor

A

platelets, neutrophils, basophils, mast cells, macrophages, endothelial cells (NOT lymphocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Stimulation for Platelet activating factor formation

A

stimulation of cells of origin, bacterial endotoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Actions of Platelet activating factor

A

platelet activation/stimulation, vasoconstriction, low concentrations: vasodilation and vasculature permeability, chemotaxis and leukocyte activation, bronchospasm, neutrophil oxidative burst
GOAL= TO STOP BLEEDING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Reactive Oxygen Species (ROS)

A

NADPH oxidase system, superoxide anion, hydrogen peroxide, hyroxyl radical derived from phospholipids of cell membranes, can combine with NO to produce reactive nitrogen species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Sources of ROS

A

Leukocytes (e.g. macrophages, neutrophils), endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Stimulus for release of ROS

A

cytokines in response to damage, damage to endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Effects of ROS

A

microbe damage, host tissue collageral damage (endothelial/parenchymal cells), inactivation of antiproteases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Inactivation of ROS

A

liver and local enzymes: superoxide dismutates, catalase for H2O2, glutathione peroxidase, ceruloplasmin, transferrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Nitric Oxide

A

formed from nitric oxide synthase (NOS); three types: iNOS, eNOS, nNOS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

iNOS (Type II)

A

endothelium, smooth muscle, macrophages; CA INDEPENDENT

27
Q

iNOS synthesis

A

induced by cytokines IL-1/TNF/Interferon, microbial endotoxin

28
Q

eNOS (Type III)

A

Endothelial cells, constitutively expressed, regulated by cytplasmic Ca; upregulated by bradykinin, thrombin, stress

29
Q

nNOS (type I)

A

Neural parenchyma; constitutively expressed, regulated by cytoplasmic Ca, functions in neurotransmitter release and blood flow regulation

30
Q

Inactivation of NO

A

short half life, regulated by rate of synthesis

31
Q

NO function

A

in inflammation (paracrine–close proximity)– Vasodilation/blood flow regulation (i,e,n), chemotaxis (i), reduced leukocyte and platelet adhesion (e), toxic effect o nmicrobes (i), neurotransmitter release (n)

32
Q

Cytokines

A

TNF, IL1, IFN; regulatory peptides/polypeptides

33
Q

Sources of cytokines

A

multiple- macrophage, lymphocytes, endothelial cellsl

34
Q

Function of cytokines

A

autocrine: act on cells that produce agents; paracrine: act on cell in vicinity of release; endocrine: act systematically to incite acute phase reaction

35
Q

Source(s) of TNF

A

principally activated macrophages, mast cells, T lymphocytes

36
Q

source(s) of IL-1

A

macrophages, endothelial cells, some epithelial cells

37
Q

stimulus for TNF secretion

A

bacterial endotoxin, immune complex, tissue injury, other inflammatory stimuli/mediators

38
Q

effects of TNF

A

LocalL: endothelial activation/thrombogenicity, fibroblast stimulation, activation of other inflammatory cells (e.g. PMNs), stimulate acute phase reaction (endocrine-like effects); Systemic: fever, anorexia, sleepiness, liver effects (increased synthesis of proteins like C-reactive protein, alpha 1-antitrypsin, clotting factors, complement factors, ferritin, ceruloplasmin, etc)

39
Q

Sources of Interleukins

A

primarily macrophages

40
Q

stimulus for IL secretion

A

bacterial endotoxin, immune complex, tissue injury, other inflammatory stimuli/mediators

41
Q

Function of IL

A

similar to TNF: fever, chemotaxis, stimulate acute phase reaction, leukocyte activation, cytokine production, ?

42
Q

IL-1 action

A

activate other inflammatory cells (PMNs); participate in acute phase rxn; innate immunity- reaction to stimuli that injure tissue

43
Q

IL-2

A

stimulates lymphocyte multiplication

44
Q

IL-8

A

(macrophages, endothelial cells): activate/attract neutrophils; synthesized in context of IL-1 and TNF, classified with “chemokines”

45
Q

cytokines-Interferon (IFN)

A

glycoprotein;

46
Q

IFN source

A

T lymphocytes, natural killer cells

47
Q

Function of IFN

A

(mostly involved with dealing with virus); activation of inflammatory cells: macrophages/Natural killer cells, Interfere with viral replication, tumor defense role

48
Q

cytokines - chemokines

A

small proteins expressed transiently or constitutively

49
Q

source of chemokines

A

variable with subtype; macrophages, lymphocytes, mast cells, endothelial cells

50
Q

function of chemokines

A

chemotaxis, control normalmigration of inflammatory cells in tissue

51
Q

Subtypes of chemokines

A

C-X-C chemokines (one aa separating first two cysteines); C-C chemokines (adjacent cysteines); C chemokines (lack first adn third of four cysteines); CX3C chemokines (3 aa between 2 cysteines)

52
Q

C-X-C chemokines

A

Ex: IL-8: macrophage/endothelial derived; neutrophil chemotaxis/activation

53
Q

C-C chemokines

A

Ex: monocyte chemoattractant Protein (MCP-1), Macrophage inflammatory protein -1-alpha (MIP-1-alpha), RANTES (regulated and normal T-cell expressed and secreted); attract macrophages, basophils, lymphocytes, eosinophils–NOT neutrophils

54
Q

C chemokines

A

lymphotactin - attract lymphocytes

55
Q

CX3C chemokines

A

fractalkine: attract macrohpages and T lymphocytes

56
Q

Cytokines involved in acute inflammation

A

TNF, IL-1, IL-6, Chemokines

57
Q

Cytokines involved in chronic inflammation

A

IL-12, IFN-gamma, IL-17

58
Q

Two most important cytokines

A

TNF, IL-1–systemic effects

59
Q

Substance P

A

small peptide, released by nerve twigs in lung/GI

60
Q

Functions of Substance P

A

PAIN signaling, vascular tone modulation, vascular permeability modulation

61
Q

Stored Mediator Content (granules)

A

from neutrophils and macrophages for digestion of microbes/foreign material and chemotactic role

62
Q

Stored mediator content constituents

A

huge variety of enzymes (collagenase, histaminase, elastase, proteinase, nonspecific collagenases, lysosome, etc)

63
Q

Stored mediator content collateral damage/control

A

digestion of normal tissue; control - enzymes (antiproteases – liver/local production–alpha-1-antitrypsin, A2-macroglobulin)

Disease and Defense (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions