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ABSITE > 13 Inflammation and Cytokines > Flashcards

13 Inflammation and Cytokines Flashcards

1
Q

In the beginning of the inflammatory cycle - Injury causes?

A

Exposed collagen, platelet-activating factor release and tissue factor release from endothelium

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2
Q

Platelets bind to? And then?

A

Collagen release growth factors (platelet-derived growth factor) - leads to PMN and macrophage recruitment

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3
Q

What cells have the dominant role in wound healing? What do they release?

A 
Macrophages
Growth factors (PDGF) and cytokines (IL-1, TNF-a)
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4
Q

PDGF

A

Chemotactic and activates PMNs/macrophages
Chemotactic and activates fibroblasts (collagen and ECM proteins)
Angiogenesis
Epithelialization
Chemotactic for smooth muscle cells
Accelerates wound healing

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5
Q

EGF (epidermal growth factor)

A

Chemotactic and activates fibroblasts
Angiogenesis
Epithelialization

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6
Q

PAF (platelet-activating factor)

A

Generated by phospholipase in endothelium - phospholipid

Chemotatic for inflammatory cells - increased adhesion molecules

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7
Q

Factors chemotatic for inflammatory cells?

A 
PDGF
IL-8
LTB-4
C5a and C3a
PAF
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8
Q

Factors chemotatic for fibroblasts?

A

PDGF
EGF
FGF

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9
Q

Angiogenesis factors

A 
PDGF
EGF
FGF
IL-8
Hypoxia
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10
Q

Epithelialization factors

A

PDGF
EGF
FGF

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11
Q

How long to PMNs survive?

A

1-2 days in tissue

7 days in blood

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12
Q

How long do platelet survive?

A

7-10 days

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13
Q

Lymphocyte functions?

A 
Chronic inflammation (T-cells)
Antibody production (B-cells)
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14
Q

Eosinophils

A

IgE receptors that bind to allergen
Release major basic protein - stimulates basophils and mast cells to release histamine
Eosinophils are increased in parasitic infections

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15
Q

Basophils

A

Main source of histamine in blood

NOT found in tissues

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16
Q

Mast cells

A

Primary cell in type I hypersensitivity reactions

Main source of histamine in tissues

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17
Q

Histamine effects

A

Vasodilation, tissue edema, post-capillary leakage

Primary effector in type 1 HSR (allergic reactions)

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18
Q

Bradykinin effects

A

Peripheral vasodilation, increased permeability, pain, pulmonary vasoconstriction

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19
Q

Nitric oxide (NO)

A 
Arginine precursor (nitric oxide synthase)
Activates guanylate cyclase and increases cGMP, resulting in vascular smooth muscle dilation
AKA endothelium-derived relaxing factor
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20
Q

Endothelin

A

Causes vascular smooth muscle constriction

Opposite effect of nitric oxide

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21
Q

Main initial cytokine response to injury and infection?

A

Release of TNF-a and IL-1

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22
Q

What produces TNF-a

A

Macrophages

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23
Q

Effect of TNF-a

A

Increases adhesion molecules
Procoagulant
Activates neutrophils and macrophages (more cytokine production and cell recruitment)

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24
Q

What causes cachexia in patients with cancer?

A

TNF-a

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25
Q

What can high levels of TNF-a cause?

A

Circulatory collapse and multisystem organ failure

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26
Q

What produces IL-1?

A

Macrophages

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27
Q

Effects of IL-1?

A

Fever (PGE2 mediated in hypothalamus)

Raises thermal set point

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28
Q

How do NSAIDs decrease fever?

A

Reduce PGE2 synthesis - decreasing its concentration in the hypothalamus

29
Q

Why do you get fever with atelectasis?

A

Alveolar macrophages release IL-1

30
Q

IL-6

A

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

31
Q

Interferons

A

Released by lymphocytes
Target viral infection
Activate macrophages, natural killer cells and cytotoxic t-cells
Inhibit viral replication

32
Q

What is the most potent stimulus for hepatic acute phase proteins?

A

IL-6

33
Q

What increases in response to inflammation?

A 
C-reactive protein (osponin, activates complement)
Amyloid A and P
Fibringoen
Haptoglobin
Ceruloplasmin
Alpha-1 antitrypsin
C3 (complement)
34
Q

What decreases in response to inflammation?

A

Albumin
Pre-albumin
Transferrin

35
Q

Selectins

A 
L-selectins (on leukocytes)
Bind E (endothelial) and P (platelet) selectins
Causes rolling adhesion
36
Q

Beta-2 integrins

A

CD11/18 - on leukocytes
Bind ICAMs
Anchoring adhesion

37
Q

ICAM, VCAM, PECAM, ELAM

A

On endothelial cells - bind beta-2 integrin molecules on leukocytes and platelets

38
Q

What causes rolling adhesion?

A

Selectins
L- leukocytes
E - endothelial
P - platelet

39
Q

What causes anchoring adhesion?

A 
Beta-2 integrins (on leukocytes)
Binding ICAM (on endothelial cells)
40
Q

What is involved in transendothelial migration?

A

ICAM, VCAM, PECAM, ELAM

Beta-1 and 2 integrins

41
Q

What activates classic complement pathway?

A

Antigen-antibody complex - IgG or IgM

42
Q

C1, C2, C4?

A

Classic pathway

43
Q

What activates the alternative complement pathway?

A

Endotoxin, bacteria, exogenous stimuli

44
Q

B, D P (properidin)

A

Alternative pathway

45
Q

What complement factor is common to and the convergence point for both pathways?

A

C3

46
Q

What cofactor is required for both complement pathways?

A

Magnesium

47
Q

Which complement factors are anaphylatoxins?

A

C3a, C4a, C5a
Increase vascular permability
Bronchoconstriction
Activate mast cells and basophils

48
Q

What makes up the membrane attack complex?

A

C5b-9b
Causes cell lysis by creating hole in cell membrane
Attacks bacteria

49
Q

Opsonization

A

Targets antigen for immune response

C3b, C4b

50
Q

Complement which is chemotaxis for inflammatory cells

A

C3a, C5a

51
Q

Prostaglandins are produced from

A

Arachidonic precursors

52
Q

Effects of PGI2/PGE2?

A

Vasodilation
Bronchodilation
Increased permeability
Inhibits platelets

53
Q

Effect of NSAIDs

A

Inhibits cycloxygenase

Reversible

54
Q

Effect of Aspirin

A

Inhibits cyclooxygenase
Irreversible
Inhibits platelet adhesion by decreasing TXA2

55
Q

Effect of steroids on inflammation

A

Inhibit phospholipase, which converts phospholipids to arachidonic acid
Therefore, inhibits inflammation

56
Q

Source of leukotrienes

A

Arachidonic precursors

57
Q

What are the slow-reacting substance of anaphylaxis?

What do theycause?

A 
LTC4, LTD4, LTE4
Bronchoconstriction
Vasoconstriction
Followed by increased permeability 
(Wheal and flare)
58
Q

Effect of LTB4

A

Chemotatic for inflammatory cells

59
Q

When do catecholamines peak after injury?

A

24-48hrs

60
Q

Where is epinephrine released from?

A

Adrenal medulla

Postganglionic neurons

61
Q

Where is norepinephrine released from?

A

Adrenal medulla

62
Q

What is the neuroendocrine response to injury?

A

Efferent nerves from site of injury stimlate CRF, ACTH, ADH, growth hormone, epinephrine and noreepinephrine release

63
Q

What is thyroid hormone’s role in injury or inflammation?

A

NOTHING

64
Q

What are the CXC chemokines? What do they do?

A

IL-8, Platelet factor 4
Chemotaxis, angiogenesis, wound healing
C = Cysteine, X = another amino acid

65
Q

What oxidants are generated in inflammation?

A 
Superoxide anion radical (NADPH oxidase)
Hydrogen peroxide (xanthine oxidase)
66
Q

What are the cellular defenses against oxidative species?

A

Superoxide anion radical (superoxide dismutase)
Converts to hydrogen peroxide
Hydrogen peroxide (Glutathione peroxidase, vatalase)

67
Q

What is the primary mediator of reperfusion injury?

A

PMNs

68
Q

Chronic granulomatous disease

A

NADPH-oxidase system enzyme defect in PMNs

Results in decreased superoxide radical formation

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