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Drafts of absite from online deck > Chapter 13: Inflammation and Cytokines > Flashcards

Chapter 13: Inflammation and Cytokines Flashcards

1
Q

Leads to exposed collagen, platelet-activating factor release and tissue factor release from endothelium

A

Injury

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2
Q

What happens when platelets bind collagen?

A

Release growth factors (platelet-derived growth factor [PDGF]); leads to PMN and macrophage recruitment

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3
Q

Dominant role in wound healing; release important growth factors (PDGF) and cytokines (IL-1 and TNF-alpha)

A

Macrophages

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4
Q
  • Chemotactic and activates inflammatory cells (PMNs and macrophages)
  • Chemotactic and activates fibroblasts -> collagen and ECM proteins
  • Angiogenesis, epithelialization, chemotactic for smooth muscle cells, has been shown to accelerate wound healing
A

PDGF

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5
Q
  • Chemotactic and activates fibroblasts
  • Angiogenesis
  • Epithelialization
A

EGF (epidermal growth factor)

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6
Q
  • Chemotactic and activates fibroblasts -> collagen and ECM proteins
  • Angiogenesis
  • Epithelialization
A

FGF (fibroblastic growth factor)

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7
Q
  • Is not stored, generated by phospholipase in endothelium; is a phospholipid
  • Chemotactic for inflammatory cells; increase adhesion molecules
A

PAF (platelet-activating factor)

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8
Q

Chemotactic factors: for inflammatory cells

A

PDGF, IL-8, LTB-4, C5a and C3a, PAF

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9
Q

Chemotactic factors: for fibroblasts

A

PDGF, EGF, FGF

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10
Q

Angiogenesis factors

A

PDGF, EGF, FGF, IL-8, hypoxia

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11
Q

Epithelialization factors

A

PDGF, EGE, FGF

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12
Q

Last 1-2 days in tissues (7 days in blood)

A

PMNs

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13
Q

Lasts 7-10 days

A

Platelets

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14
Q

Involved in chronic inflammation (T cells) and antibody production (B cells)

A

Lymphocytes

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15
Q

Growth and activating factors

A

PDGF, EGF, FGF, PAF, (Chemotactic, angiogenesis, epithelialization), PMNs, platelets, lymphocytes, TXA2, PGI2

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16
Q
  • Have IgE receptors that bind to allergen
  • Release major basic protein, which stimulates basophils and mast cells to release histamine
  • Increased in parasitic infections
A

Eosinophils

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17
Q

What do eosinophils release?

A

Major basic protein, which stimulates basophils and mast cells to release histamine

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18
Q

Main source of histamine in blood; not found in tissue

A

Basophils

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19
Q
  • Primary cell in type 1 hypersensitivity reactions

- Main source of histamine in tissues

A

Mast cells

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20
Q
  • Vasodilation, tissue edema, postcapillary leakage

- Primary effector in type 1 hypersensitivity reactions (allergic reactions)

A

Histamine

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21
Q

Peripheral vasodilation, increased permeability, pain, pulmonary vasoconstriction

A

Bradykinin

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22
Q

Inactivates bradykinin; located in lung

A

Angiotensin-converting enzyme (ACE)

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23
Q

Cells involved in type 1 hypersensitivity reactions

A

Eosinophils, basophils, mast cells, histamine, bradykinin

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24
Q

Substrate for nitric oxide synthase

A

Arginine

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25
Activates gauntlet cyclase and increases cGMP, resulting in vascular smooth muscle dilation - AKA: endothelium-derived relaxing factor
Nitric Oxide (NO)
26
Causes vascular smooth muscle constriction (opposite effect of nitric oxide)
Endothelin
27
Main initial cytokine response to injury and infection
TNF-alpha and IL-1
28
Largest producers of TNF
Macrophages
29
- Increases adhesion molecules - Overall, a procoagulant. - Causes cachexia in patients with cancer. - Activates neutrophils and macrophages
TNF-alpha
30
What can high concentrations of TNF-alpha cause?
Circulatory collapse and multisystem organ failure
31
- Main source macrophages; effects similar to TNF-alpha and synergizes TNF-alpha - Responsible for fever (PGE2 mediated in hypothalamus)
IL-1
32
Cause fever with atelectasis by releasing IL-1
Alveolar macrophages
33
Increases hepatic acute phase proteins (C-reactive protein, amyloid A)
IL-6
34
- Released by lymphocytes in response to viral infection or other stimulants - Active macrophages, natural killer cells, and cytotoxic T cells - Inhibit viral replication
Interferon
35
Most potent stimulus for hepatic acute phase response proteins
IL-6
36
Hepatic acute phase response proteins - Increased? - Decreased?
- Increased: CRP, amyloid A and P, fibrinogen, haptoglobin, ceruloplasmin, alpha-1 antitrypsin, and C3 (complement - Decreased: albumin, pre-albumin, and transferrin
37
An opsonin, activates complement
C-reactive protein
38
- On leukocytes - Bind ICAMs, etc - Anchoring adhesion
Beta-2 integrins (CD 11/18 molecules)
39
- On endothelial cells, bind beta-2 integrin molecules located on leukocytes and platelets - Also involved in transendothelial migration
ICAM, VCAM, PECAM, ELAM
40
What activates the classic complement pathway (IgG, or IgM)?
Antigen-antibody complex activates
41
Factors found only in the classic pathway
Factors C1, C2, and C4
42
What activates the alternative complement pathway?
Endotoxin, bacteria, other stimuli activate
43
Factors found only in the alternative pathway
Factors B, D, and P (properdin)
44
Complement: common to and is the convergence point for both pathway (alternative and classic)
C3
45
Complement: required for both pathways
Magnesium
46
- Increase vascular permeability, bronchoconstriction | - Activate mast cells and basophils
Anaphylatoxins (C3a, C4a, C5a)
47
What is the membrane attack complex?
C5b-9b, causes cell lysis (usually bacteria) by creating a hole in the cell membrane
48
Complement: opsonization (targets antigen for immune response)
C3b and C4b
49
Complement: chemotaxis for inflammatory cells
C3a and C5a
50
Produced from arachidonic precursors
Prostaglandins, Leukotrienes
51
Prostaglandins: - Vasodilation - Bronchodilation - Increased permeability - Inhibits platelets
PGI-2 and PGE-2
52
Inhibits cyclooxygenase (reversible)
NSAIDs
53
Inhibits cyclooxygenase (irreversible), inhibits platelet adhesion by decreasing TXA2
Aspirin
54
Inhibits phospholipase, which converts phospholipids to arachidonic acid -> inhibits inflammation
Steroids
55
Leukotrienes: slow-reacting substances of anaphylaxis; bronchoconstriction, vasoconstriction followed by increased permeability (wheal and flare)
LTC-4, LTD-4, LTE-4
56
Leukotrienes: chemotactic for inflammatory cells
LTB-4
57
Peaks 24-48 hours after injury
Catecholamines
58
Released from sympathetic postganglionic neurons
Norepinephrine
59
Released from the adrenal medulla (neural response to injury)
Epinephrine and norepinephrine
60
Neuroendocrine response to injury
Afferent nerves from site of injury stimulate CRF, ACTH, ADH, GH, epinephrine, and norepinephrine release
61
Does not play a major role in injury or inflammation
Thyroid hormone
62
Function: CXC chemokines
Chemotaxis, angiogenesis, wound healing
63
What are IL-8 and platelet factor 4?
``` CXC chemokines (C = cysteine, X = another amino acid) ```
64
Generated in inflammation
Oxidants
65
Main producer: superoxide anion radical (O2-)
NADPH oxidase
66
Main producer: Hydrogen peroxidase (H2O2)
Xanthine Oxidase
67
Cellular defense: superoxide anion radical
Superoxide dismutase
68
Cellular defense: hydrogen peroxidase
Glutathione peroxidase, catalase
69
Primary mediator of reperfusion injury
PMNs
70
NADPH-oxidase system enzyme defect in PMNs | - Results in decreased superoxide radical (O2-) formation
Chronic Granulomatous Disease

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