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MOD > Chapter 3 Part 2 > Flashcards

Chapter 3 Part 2 Flashcards

1
Q

Histamine

A

Source: mast cells, basophils, platelets
Action: vasodilation, increased vascular permeability, endothelial activation

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2
Q

Prostaglandins

A

Source: mast cells, leukocytes
Action: vasodilation, pain, fever

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3
Q

Leukotrienes

A

Source: mast cells, leukocytes
Action: increased vascular permeability, chemotaxis, leukocyte adhesion, and activation

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4
Q

Cytokines (TNF, IL-6, IL-1)

A

Source: macrophages, endothelial cells, mast cells
Local Action: endothelial activation (expression of adhesion molecules)
Systemic Action: fever, metabolic abnormalities, hypotension (shock)

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5
Q

Chemokines

A

Source: leukocytes, activated macrophages
Action: chemotaxis, leukocyte activation

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6
Q

Platelet-activating Factor

A

Source: leukocytes, mast cells
Action: vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst

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7
Q

Complement

A

Source: plasma (produced in liver)
Action: leukocyte chemotaxis and activation, fireteams target killing (membrane attack complex), vasodilation (mast cell stimulation)

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8
Q

Kinins

A

Source: plasma (produced in liver)
Action: increased vascular permeability, smooth muscle contraction, vasodilation, pain

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9
Q

What are the most important mediators of acute inflammation?

A

vasoactive amines, lipid products (prostaglandins and leukotrienes), cytokines (including chemokines), products of complement activation

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10
Q

Cell-derived mediators

A

sequestered in intracellular granules and can be rapidly secreted by granule exocytosis or are synthesized de novo
ex) histamine in mast cell granules

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11
Q

Major cell types that produce mediators of acute inflammation

A

macrophages, dendritic cells, mast cells

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12
Q

Plasma-derived mediators

A

produced mainly in the liver and are present in circulation as inactive precursors that must be activated
ex) complement proteins

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13
Q

2 major vasoactive amines

A

histamine

serotonin

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14
Q

Histamine: storage, release, and action

A

Storage: mast cell granules
Release: mast cell degranulation in response to 1) physical injury; 2) binding of antibodies to mast cell; 3) products of complement (C3a and C5a); 4) neuropeptides, cytokine (IL-1, IL-8)
Action: dilation of arterioles and increased permeability of venules via H1 receptor binding

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15
Q

Serotonin: storage, release, action

A

Storage: preformed in platelets and neuroendocrine cells
Action: neurotransmitter in GI tract, vasoconstrictor

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16
Q

What two lipid mediators are produced from Arachidonic Acid?

A

Prostaglandins

Leukotrienes

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17
Q

What is AA made of?

A

20-carbon unsaturated fatty acid from diet or essential fatty acid linoleum acid esterified in membrane phospholipids

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18
Q

Release of AA

A

mechanical, chemical, physical mediators release AA from membrane phospholipids via action of phospholipase A2

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19
Q

What two major classes of enzymes do eicosanoids (AA-derived mediators) synthesize?

A

Cyclooxygenases: generate prostaglandins
Lipoxygenases: produce leukotrienes and lipoxins

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20
Q

What do steroids inhibit?

A

phospholipase (inhibit release of AA)

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21
Q

What do COX-1 and COX-2 inhibitors, aspirin, and indomethacin inhibit?

A

cyclooxygenase (production of prostaglandins)

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22
Q

Prostacyclin PGI2 action

A

vasodilation, inhibits platelet aggregation

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23
Q

Thromboxane A2 (TXA2) action

A

vasoconstriction, promotes platelet aggregation

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24
Q

PGD2, PGE2 actions

A

vasodilation, increased vascular permeability

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25
Q

5-HETE action

A

chemotaxis

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26
Q

Leukotriene C4, D4, E4 (LTC4, LTD4, LTE4) actions

A

bronchospasm, increased vascular permeability

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27
Q

Lipoxin A4, B4 (LXA4, LXB4) actions

A

inhibition of inflammation

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28
Q

What do leukotriene receptor antagonists inhibit?

A

bronchospasm produced by LTC4, LTD4, LTE4

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29
Q

Which eicosanoids cause vasodilation?

A

Prostaglandins PGI2, PGE1, PGE2, PGD2

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30
Q

Which eicosanoids cause vasocontriction?

A

Thromboxane A2, Leukotrienes C4, D4, E4

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31
Q

Which eicosanoids cause increased vascular permeability?

A

Leukotrienes C4, D4, E4

32
Q

Which eicosanoids cause chemotaxis and leukocyte adhesion?

A

Leukotriene B4, HETE

33
Q

COX-1

A

produced in response to inflammatory stimuli and constitutively expressed in most tissues, where it may serve a homeostatic function

34
Q

COX-2

A

produced by inflammatory stimuli, but low or absent in most tissues

35
Q

What has a thromboxane-prostacyclin imbalance been implicated as an early event in?

A

thrombus formation in coronary and cerebral vessels

36
Q

Systemic effects of prostaglandins

A

fever, pain

37
Q

Leukotriene: source and action

A

Source: produced by leukocytes and mast cells by lipoxygenase action
Action: vascular and smooth muscle reactions and leukocyte recruitment

38
Q

Role of 5-lipoxygenase

A

predominant lipoxygenase in neutrophils; converts AA to 5-HPETE, which is precursor for leukotrienes and chemotactic for neutrophils

39
Q

Which are more potent in increasing vascular permeability and causing bronchospasm, histamine or leukotrienes?

A

Leukotrienes

40
Q

Lipotoxins: source and action

A

Source: generated from AA by lipoxygenase pathway
Action: suppress inflammation by inhibiting the recruitment of leukocytes, inhibits neutrophil chemotaxis and adhesion; require 2 cell populations for transcellular biosynthesis (leukocytes produce intermediates that are converted to lipoxins by platelets)

41
Q

Actions of COX inhibitors

A

inhibit prostaglandin synthesis (treat fever and pain); aspirin does this by irreversibly acetylating and inactivating cyclooxygenases

42
Q

Actions of Lipoxygenase inhibitors

A

5-lipoxygenase not affects by NSAIDS; inhibit leukotriene production (useful for treating asthma)

43
Q

Actions of corticosteroids

A

antiinflammatory; reduce transcription of gene encoding COX-2, phospholipase A2, pro inflammatory cytokines (IL-1 and TNF), and iNOS

44
Q

Actions of leukotriene receptor antagonists

A

block and prevent actions of leukotrienes (asthma treatment)

45
Q

What does consumption of fish oil do?

A

polyunsaturated fats are poor substrates for conversion to active metabolites by cyclooxygenase and lipoxygeanse pathways, but better for production of anti-inflammatory lipid products

46
Q

Cytokines: source and action

A

Source: produced by many cell types and activated by lymphocytes, macrophages, dendritic cells, endothelial and epithelial cells, and connective tissue cells
Actions: mediate and regulate immune and inflammatory reactions

47
Q

TNF and IL-1: source, stimulation, and actions

A

Source: produced by activated macrophages and dendritic cells (TNF also produced by T lymphocytes; IL-1 also produced by some epithelial cells)
Stimulation: microbial products, immune complexes, foreign bodies, physical injury; TNF induced by signals through TLRs and microbial sensors; IL-1 activation dependent on inflammasome
Actions: endothelial activation (increased expression of adhesion molecules, increased production of mediators, increased procoagulant activity); activation of leukocytes and other cells (TNF induces production of NO; IL-1 activates fibroblasts, and stimulates Th17 responses); systemic acute-phase response (fever, suppress appetite)

48
Q

TNF antagonists actions

A

treatment of chronic inflammatory diseases; patients become susceptible to mycobacterial infection due to reduced ability of macrophages to kill intracellular microbes

49
Q

IL-6

A

Source: macrophages
Actions: systemic effects (acute phase response)

50
Q

Chemokines

A

Source: macrophages, endothelial cells, T lymphocytes, was cells
Actions: recruitment of leukocytes to sites of inflammation; migration of cells in normal tissues

51
Q

IL-17

A

Source: T lymphocytes
Actions: recruitment of neutrophils and monocytes

52
Q

IL-12

A

Source: dendritic cells, macrophages
Actions: increased production IFN-y

53
Q

IFN-y

A

Source: T-lymphocytes, NK cells
Actions: activation of macrophages

54
Q

C-X-C chemokines

A

act on neutrophils
IL-8
induced by IL-1 and TNF

55
Q

C-C chemokines

A

MCP-1, eotaxin, MIP-1a, RANTES

attract monocytes, eosinophils, basophils, and lymphocytes

56
Q

C chemokines

A

specific for lymphocytes

57
Q

Cx3C chemokines

A

fractaline
cell surface bound- promotes strong adhesion of monocytes and T cells
soluble form- chemoattractant activity

58
Q

Chemokine functions

A

stimulate leukocyte attachment to endothelium by increasing leukocyte affinity of integrins and stimulate chemotaxis (inflammatory); homeostatic chemokines maintain tissue architecture

59
Q

What is the complement system a collection of?

A

soluble proteins and membrane receptions that function mainly in host defense against microbes and in pathologic inflammatory reactions

60
Q

What is the critical step in complement activation?

A

proteolysis of C3

61
Q

Classical Pathway

A

triggered by fixation of C1 to IgM or IgG antibody that has combined with antigen

62
Q

Alternative Pathway

A

triggered by microbial surface molecules, complex polysaccharides, cobra venom, and other substances in absence of antibody

63
Q

Lectin Pathway

A

plasma mannose-binding lectin binds to carbohydrates on microbes and directly activates C1

64
Q

Steps on complement pathway:

A

1) activation leads to C3 converts formation
2) splits into C3a and C3b
3) C3a released
4) C3b attaches to cell or molecule where complement is being activated
5) more C3b fragments come together to form C5 converts
6) cumulation of steps leading to MAC formation

65
Q

Main functions of complement system (3)

A

Inflammation- C3a, C5a, C4a
Opsonization and phagocytosis- C3b
Cell Lysis- MAC deposition

66
Q

C1 inhibitor (C1 INH)

A

blocks activation of C1; inherited deficiency is the cause of hereditary angioedema

67
Q

Decay Accelerating Factor (DAF) and CD59

A

linked to plasma membrane by glycophosphatidyl anchor; DAF inhibits formation of C3 convertase; CD59 inhibits formation of MAC; deficiency leads to paroxysmal nocturnal hemoglobinuria

68
Q

PAF

A

platelet aggregation, inflammatory effects, vasoconstriction and bronchoconstriction (at low concentrations induces vasodilation and increased venular permeability)

69
Q

PARs

A

protease activated receptors; activated by thrombin to produce fibrin (form clot), expressed on platelets and leukocytes

70
Q

Kinins

A

vasoactive peptides derived from plasma proteins, kininogens, by action of kallikreins (proteases)

71
Q

Bradykinin

A

increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and pain when injected into the skin (mediator in some forms of allergic reaction)

72
Q

Neuropeptides (substance P and neurokinin A)

A

secreted by sensory nerves and various leukocytes; may play role in initiation and regulation of inflammatory response

73
Q

Morphologic hallmarks of acute inflammatory reactions

A

dilation of small blood vessels, accumulation of leukocytes and fluid in extravascular tissue

74
Q

Serous Inflammation

A

exudation of cell-poor fluid into spaces created by cell injury or into body cavities lines by peritoneum, pleura, or pericardium (effusion)

75
Q

Fibrinous Inflammation

A

fibrinogen leakage out of blood and formation of fibrin deposits in extracellular space; fibrinous exudate develops when vascular leaks are large or there is a local procoagulant stimulus

  • formation of scars
  • seen in lining of body cavities, such as meninges and pericardium
76
Q

Purulent (suppurative) Inflammation, Abscess

A

production of pus, an exudate consisting of neutrophils, the liquefied debris of necrotic cells, and edema fluid (bacterial infection- staph); abscesses are localized collections of purulent inflammatory tissues

77
Q

Ulcers

A

local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing of inflamed necrotic tissue

MOD (34 decks)

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