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My Absite > 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
Q

Activates gauntlet cyclase and increases cGMP, resulting in vascular smooth muscle dilation
- AKA: endothelium-derived relaxing factor

A

Nitric Oxide (NO)

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26
Q

Causes vascular smooth muscle constriction (opposite effect of nitric oxide)

A

Endothelin

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27
Q

Main initial cytokine response to injury and infection

A

TNF-alpha and IL-1

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28
Q

Largest producers of TNF

A

Macrophages

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29
Q
  • Increases adhesion molecules
  • Overall, a procoagulant.
  • Causes cachexia in patients with cancer.
  • Activates neutrophils and macrophages
30
Q

What can high concentrations of TNF-alpha cause?

A

Circulatory collapse and multisystem organ failure

31
Q
  • Main source macrophages; effects similar to TNF-alpha and synergizes TNF-alpha
  • Responsible for fever (PGE2 mediated in hypothalamus)
32
Q

Cause fever with atelectasis by releasing IL-1

A

Alveolar macrophages

33
Q

Increases hepatic acute phase proteins (C-reactive protein, amyloid A)

34
Q
  • Released by lymphocytes in response to viral infection or other stimulants
  • Active macrophages, natural killer cells, and cytotoxic T cells
  • Inhibit viral replication
A

Interferon

35
Q

Most potent stimulus for hepatic acute phase response proteins

36
Q

Hepatic acute phase response proteins

  • Increased?
  • Decreased?
A
  • Increased: CRP, amyloid A and P, fibrinogen, haptoglobin, ceruloplasmin, alpha-1 antitrypsin, and C3 (complement
  • Decreased: albumin, pre-albumin, and transferrin
37
Q

An opsonin, activates complement

A

C-reactive protein

38
Q
  • On leukocytes
  • Bind ICAMs, etc
  • Anchoring adhesion
A

Beta-2 integrins (CD 11/18 molecules)

39
Q
  • On endothelial cells, bind beta-2 integrin molecules located on leukocytes and platelets
  • Also involved in transendothelial migration
A

ICAM, VCAM, PECAM, ELAM

40
Q

What activates the classic complement pathway (IgG, or IgM)?

A

Antigen-antibody complex activates

41
Q

Factors found only in the classic pathway

A

Factors C1, C2, and C4

42
Q

What activates the alternative complement pathway?

A

Endotoxin, bacteria, other stimuli activate

43
Q

Factors found only in the alternative pathway

A

Factors B, D, and P (properdin)

44
Q

Complement: common to and is the convergence point for both pathway (alternative and classic)

45
Q

Complement: required for both pathways

46
Q
  • Increase vascular permeability, bronchoconstriction

- Activate mast cells and basophils

A

Anaphylatoxins (C3a, C4a, C5a)

47
Q

What is the membrane attack complex?

A

C5b-9b, causes cell lysis (usually bacteria) by creating a hole in the cell membrane

48
Q

Complement: opsonization (targets antigen for immune response)

A

C3b and C4b

49
Q

Complement: chemotaxis for inflammatory cells

A

C3a and C5a

50
Q

Produced from arachidonic precursors

A

Prostaglandins, Leukotrienes

51
Q

Prostaglandins:

  • Vasodilation
  • Bronchodilation
  • Increased permeability
  • Inhibits platelets
A

PGI-2 and PGE-2

52
Q

Inhibits cyclooxygenase (reversible)

53
Q

Inhibits cyclooxygenase (irreversible), inhibits platelet adhesion by decreasing TXA2

54
Q

Inhibits phospholipase, which converts phospholipids to arachidonic acid -> inhibits inflammation

55
Q

Leukotrienes: slow-reacting substances of anaphylaxis; bronchoconstriction, vasoconstriction followed by increased permeability (wheal and flare)

A

LTC-4, LTD-4, LTE-4

56
Q

Leukotrienes: chemotactic for inflammatory cells

57
Q

Peaks 24-48 hours after injury

A

Catecholamines

58
Q

Released from sympathetic postganglionic neurons

A

Norepinephrine

59
Q

Released from the adrenal medulla (neural response to injury)

A

Epinephrine and norepinephrine

60
Q

Neuroendocrine response to injury

A

Afferent nerves from site of injury stimulate CRF, ACTH, ADH, GH, epinephrine, and norepinephrine release

61
Q

Does not play a major role in injury or inflammation

A

Thyroid hormone

62
Q

Function: CXC chemokines

A

Chemotaxis, angiogenesis, wound healing

63
Q

What are IL-8 and platelet factor 4?

A 
CXC chemokines
(C = cysteine, X = another amino acid)
64
Q

Generated in inflammation

65
Q

Main producer: superoxide anion radical (O2-)

A

NADPH oxidase

66
Q

Main producer: Hydrogen peroxidase (H2O2)

A

Xanthine Oxidase

67
Q

Cellular defense: superoxide anion radical

A

Superoxide dismutase

68
Q

Cellular defense: hydrogen peroxidase

A

Glutathione peroxidase, catalase

69
Q

Primary mediator of reperfusion injury

70
Q

NADPH-oxidase system enzyme defect in PMNs

- Results in decreased superoxide radical (O2-) formation

A

Chronic Granulomatous Disease

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