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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
5-HETE action
chemotaxis
26
Leukotriene C4, D4, E4 (LTC4, LTD4, LTE4) actions
bronchospasm, increased vascular permeability
27
Lipoxin A4, B4 (LXA4, LXB4) actions
inhibition of inflammation
28
What do leukotriene receptor antagonists inhibit?
bronchospasm produced by LTC4, LTD4, LTE4
29
Which eicosanoids cause vasodilation?
Prostaglandins PGI2, PGE1, PGE2, PGD2
30
Which eicosanoids cause vasocontriction?
Thromboxane A2, Leukotrienes C4, D4, E4
31
Which eicosanoids cause increased vascular permeability?
Leukotrienes C4, D4, E4
32
Which eicosanoids cause chemotaxis and leukocyte adhesion?
Leukotriene B4, HETE
33
COX-1
produced in response to inflammatory stimuli and constitutively expressed in most tissues, where it may serve a homeostatic function
34
COX-2
produced by inflammatory stimuli, but low or absent in most tissues
35
What has a thromboxane-prostacyclin imbalance been implicated as an early event in?
thrombus formation in coronary and cerebral vessels
36
Systemic effects of prostaglandins
fever, pain
37
Leukotriene: source and action
Source: produced by leukocytes and mast cells by lipoxygenase action Action: vascular and smooth muscle reactions and leukocyte recruitment
38
Role of 5-lipoxygenase
predominant lipoxygenase in neutrophils; converts AA to 5-HPETE, which is precursor for leukotrienes and chemotactic for neutrophils
39
Which are more potent in increasing vascular permeability and causing bronchospasm, histamine or leukotrienes?
Leukotrienes
40
Lipotoxins: source and action
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
Actions of COX inhibitors
inhibit prostaglandin synthesis (treat fever and pain); aspirin does this by irreversibly acetylating and inactivating cyclooxygenases
42
Actions of Lipoxygenase inhibitors
5-lipoxygenase not affects by NSAIDS; inhibit leukotriene production (useful for treating asthma)
43
Actions of corticosteroids
antiinflammatory; reduce transcription of gene encoding COX-2, phospholipase A2, pro inflammatory cytokines (IL-1 and TNF), and iNOS
44
Actions of leukotriene receptor antagonists
block and prevent actions of leukotrienes (asthma treatment)
45
What does consumption of fish oil do?
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
Cytokines: source and action
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
TNF and IL-1: source, stimulation, and actions
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
TNF antagonists actions
treatment of chronic inflammatory diseases; patients become susceptible to mycobacterial infection due to reduced ability of macrophages to kill intracellular microbes
49
IL-6
Source: macrophages Actions: systemic effects (acute phase response)
50
Chemokines
Source: macrophages, endothelial cells, T lymphocytes, was cells Actions: recruitment of leukocytes to sites of inflammation; migration of cells in normal tissues
51
IL-17
Source: T lymphocytes Actions: recruitment of neutrophils and monocytes
52
IL-12
Source: dendritic cells, macrophages Actions: increased production IFN-y
53
IFN-y
Source: T-lymphocytes, NK cells Actions: activation of macrophages
54
C-X-C chemokines
act on neutrophils IL-8 induced by IL-1 and TNF
55
C-C chemokines
MCP-1, eotaxin, MIP-1a, RANTES | attract monocytes, eosinophils, basophils, and lymphocytes
56
C chemokines
specific for lymphocytes
57
Cx3C chemokines
fractaline cell surface bound- promotes strong adhesion of monocytes and T cells soluble form- chemoattractant activity
58
Chemokine functions
stimulate leukocyte attachment to endothelium by increasing leukocyte affinity of integrins and stimulate chemotaxis (inflammatory); homeostatic chemokines maintain tissue architecture
59
What is the complement system a collection of?
soluble proteins and membrane receptions that function mainly in host defense against microbes and in pathologic inflammatory reactions
60
What is the critical step in complement activation?
proteolysis of C3
61
Classical Pathway
triggered by fixation of C1 to IgM or IgG antibody that has combined with antigen
62
Alternative Pathway
triggered by microbial surface molecules, complex polysaccharides, cobra venom, and other substances in absence of antibody
63
Lectin Pathway
plasma mannose-binding lectin binds to carbohydrates on microbes and directly activates C1
64
Steps on complement pathway:
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
Main functions of complement system (3)
Inflammation- C3a, C5a, C4a Opsonization and phagocytosis- C3b Cell Lysis- MAC deposition
66
C1 inhibitor (C1 INH)
blocks activation of C1; inherited deficiency is the cause of hereditary angioedema
67
Decay Accelerating Factor (DAF) and CD59
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
PAF
platelet aggregation, inflammatory effects, vasoconstriction and bronchoconstriction (at low concentrations induces vasodilation and increased venular permeability)
69
PARs
protease activated receptors; activated by thrombin to produce fibrin (form clot), expressed on platelets and leukocytes
70
Kinins
vasoactive peptides derived from plasma proteins, kininogens, by action of kallikreins (proteases)
71
Bradykinin
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
Neuropeptides (substance P and neurokinin A)
secreted by sensory nerves and various leukocytes; may play role in initiation and regulation of inflammatory response
73
Morphologic hallmarks of acute inflammatory reactions
dilation of small blood vessels, accumulation of leukocytes and fluid in extravascular tissue
74
Serous Inflammation
exudation of cell-poor fluid into spaces created by cell injury or into body cavities lines by peritoneum, pleura, or pericardium (effusion)
75
Fibrinous Inflammation
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
Purulent (suppurative) Inflammation, Abscess
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
Ulcers
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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