3. Chemical Mediators of Inflammation. Flashcards

1
Q

What are the 2 groups that chemical mediators are divided into?

A

Those that are derived from cells and those that are derived from plasma.

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2
Q

What are cellular chemical mediators?

A

Pre-made substances that are located in the cytoplasm of a cell.

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3
Q

When are cellular chemical mediators released?

A

Following the stimulation or lysis of that cell.

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4
Q

What are 4 examples of cellular chemical mediators?

A

Lipid Mediators.

Vasoactive amines.

Cytokines and chemokines.

Lysosomal contents from phagocytic cells.

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5
Q

What are plasma chemcial mediators?

A

Soluble factors that are found in the blood stream.

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6
Q

How are plasma chemcial mediators interconnected?

A

Via a cascade system, this means that when one subunit gets activated it then activates another and so on.

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7
Q

Lipid mediators are involved in what pathway?

A

The arachidonic acid pathway.

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8
Q

What enzyme is upregulated when there is damage to the PPL bilayer on cell membranes?

A

Phospholipase A2.

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9
Q

What is the function of phospholipase A2?

A

It breaks down the phospholipid bilayer and this forms arachidonic acid.

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10
Q

What happens to the arachidonic acid that is formed by the destruction of the cell membrane by phospholipase A2?

A

It is broken down by the cyclooxegenase pathway or the lipooxegenase pathway.

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11
Q

What enzymes break down arachidonic acid in the cyclooxegenase pathway ?

A

Cyclooxegenase-1 (COX-1).

Cyclooxegenase-2 (COX-2).

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12
Q

What is made by COX-1?

A

Thromboxanes and prostaglandins

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13
Q

What is made by COX-2?

A

Prostaglandins.

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14
Q

What is made by the lipooxegenase pathway?

A

Leukotrienes.

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15
Q

What is the role of COX-1 in healthy animals?

A

It helps with the protection of mucosal cells and renal function.

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16
Q

When are levels of COX-1 increased?

A

During inflammation.

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17
Q

When is COX-2 expressed?

A

During inflammation.

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18
Q

What is the role of the thrombaxanes that are upregulated during inflammation?

A

They produce vasoconstriction and platelet aggregation.

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19
Q

What are the 5 things produced by prostaglandins during inflammation?

A

Fever.

Pain.

Vasodilation.

Increased vascular permeability.

Leukocyte adhesion and chemotaxis.

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20
Q

How do NSAIDs affect inflammation?

A

They reduce the up regulation of COX-1 and COX-2.

This reduces the amount of thromboxane and prostaglandins.

This results in less redness, swelling, heat and pain.

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21
Q

What changes do we often see if we put an animal of NSAIDs for a long time and why do these changes occur?

A

Reduced renal function and reduced protection in mucosal areas.

As COX-1 enzymes are active in healthy animals and they are suppressed by NSAIDs.

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22
Q

Leukotrienes are involved in what kind of reactions?

A

Hypersensitivity and allergic reactions.

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23
Q

What are the 4 things that leukotrienes can cause in the body?

A

Smooth muscle contraction.

Vasodilation.

Leukocyte adhesion and chemotaxis.

Mucous secretion.

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24
Q

Do leukotrienes or histamine have a more potent response?

A

Leukotrienes are more potent but have a less rapid response.

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25
Q

What produces platelet activating factor following damage to the cell membrane?

A

Phospholipase A2.

Platelet activating factor is a lipid mediator.

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26
Q

What is the most potent activator of vascular permeability?

A

Platelet activating factor.

This means it increases the size of gap junctions in the vascular endothelium.

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27
Q

What are the 2 things that occur once platelet activating factor has been activated?

A

WBC chemotaxis and activation.

Platelet activation.

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28
Q

What are leukocytes?

A

White blood cells.

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29
Q

What is suppressed when an animal is given corticosteroids?

A

Phospholipase A2.

This causes widespread reduction of inflammation.

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30
Q

Do NSAIDs or corticosteroids have a better reduction of inflammation?

A

Corticosteroids, but they have more side effects.

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31
Q

What are 5 side effects of glucocorticoids?

A

Decreased mucosal protection.

Increased thirst and urination.

Increased blood sugar.

Panting and restlessness

Immunosuppression.

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32
Q

What are 3 examples of vasoactive amines?

A

Histamine.

Serotonin.

Nitric Oxide.

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33
Q

What are the 3 main cells that produce histamine?

A

Mast cells.

Basophils.

Platelets.

34
Q

What cells produce serotonin?

A

Platelets.

35
Q

What 2 cell types produce nitric oxide?

A

Macrophages.

Endothelial cells.

36
Q

Do vasoactive amines act locally or systemically?

A

Both.

37
Q

What is the result of the release of vasoactive amines?

A

Immediate vasodilation that lasts for a short time.

38
Q

Interleukins are a class of what?

A

Cytokine.

39
Q

What 4 things will interleukins and interferons respond to?

A

Infection.

Hypersensitivities.

Inflammation.

Cancer.

40
Q

What cells produce interleukins and interferons?

A

Many different cells.

41
Q

What is influenced by interleukins and interferons?

A

The innate and adaptive immune systems.

42
Q

What 4 things can activate IL-1?

A

Fever.

Neutrophilia.

Activation of endothelial cells.

Activation of phospholipase A2.

43
Q

What is stimulated by IL-1?

A

Acute phase proteins.

44
Q

What 3 things activate TNF-alpha?

A

Shock.

Activation of neutrophils.

Activation of endothelial cells.

45
Q

What is stimulated by the activation of TNF-alpha?

A

The production of other cytokines.

46
Q

What interferon causes a shift from acute to chronic inflammation?

A

Interferon gamma.

47
Q

What 2 things are activated by interferon gamma?

A

Macrophages.

Lymphocytes.

48
Q

What is the role of IL-10?

A

Immune system suppression.

49
Q

What are chemokines?

A

A subclass of cytokines that are involved in the activation of cells and in chemotaxis.

50
Q

What chemokine activates neutrophils?

A

IL-8.

51
Q

What chemokine activates eosinophils?

A

Eotaxin (CCL11).

52
Q

What 4 chemokines activate lymphocytes?

A

CCL1.

CCL2.

CCL17.

CCL20.

53
Q

What chemokine activates monocytes?

A

Monocyte chemoattractant protein 1 (MCP -1, CCL2).

54
Q

Lysosomal components are found in what 2 immune cells?

A

Neutrophils.

Macrophages.

55
Q

What are 3 examples of lysosomal components found in immune cells?

A

Reactive oxygen metabolites (free radicals).

Antimicrobial peptides

Enzymes.

56
Q

The reactive oxygen metabolites found in lysosomal components of immune cells are reactive to what inflammatory mediators?

A

Pathogens.

Host cells.

57
Q

Does thrombaoxane result in vasocontriction or vasodialtion?

A

Vasoconstriction.

58
Q

What is the complement system comprised of?

A

Activated proteins that attack pathogens and enhance inflammatory responses.

59
Q

What is the difference between binding in the classical pathway, the mannan-binding lectin pathway and the alternative pathway?

A

In the classical pathway antibodies bind to antigens.

In the mannan-binding lectin pathway lectins bind to mannose.

In the alternative pathway there is non-specific binding to the pathogen surface.

60
Q

What is mannose?

A

A common sugar found on the surfaces of pathogens

61
Q

What is activated when any one of the classical pathway, the mannan-binding lectin pathway or the alternative pathway are activated?

A

All the pathways end up forming C3-convertase which then forms the membrane attack complex.

62
Q

What is the function of the MAC?

A

It bores holes in pathogens causing fluids to leak out.

63
Q

What are the 2 anaphylatoxins on the MAC?

A

C3a.

C5a.

64
Q

What is the role of the anaphylatoxins C3a and C5a?

A

Mast cell degranulation.

Vascular dilation, increased permeability.

Leukocyte adhesion and chemotaxis.

65
Q

What is the opsonin on the MAC?

A

C3-B.

66
Q

What occurs when C3-B is activated?

A

Enhanced phagocytosis by neutrophils and macrophages.

67
Q

Why would an animal with a C3 deficiency be more at risk of developing bacterial meningitis?

A

As there is a much lower production of the subunits that form the MAC.

This means the immune response is not as effective.

68
Q

What would happen if an animals had a defect in C1?

A

The classical pathway would not work and antibodies would not bind to antigens.

69
Q

How will a C3 deficiency affect the immune response?

A

Decreased vascular response.

Reduced cellular response.

Reduced MAC response.

70
Q

How will a C3 deficiency affect the immune response?

A

The classical pathway will not work.

71
Q

When does the intrinsic pathway for clotting occur?

A

When there is a platelet plug in the subendothelium.

It always occurs when there is damaged tissue.

72
Q

How does a platelet plug activate the the intrinsic pathway for clotting?

A

It activates factor 12 which starts the cascade.

73
Q

What factor leads to the activation of the intrinsic clotting pathway?

A

Factor 7.

74
Q

What factor is activated by both the intrinsic and extrinsic pathways?

A

Factor 10 which leads to the formation of fibrin.

75
Q

What 2 things activate the enzyme kalliekrin?

A

Microbes.

Factor 12.

76
Q

What happens once kalliekrin is activated?

A

It activates kininogens which then form various kinins.

77
Q

When is the fibrinolytic system activated?

A

At the same time as the clotting cascade.

78
Q

Why is the fibrinolytic system activated at the same time as the clotting cascade?

A

To prevent thrombosis from occurring.

79
Q

Plasmin can activate what part of the clotting system?

A

C3.

80
Q

A massive intravascular immune response promotes what 2 things?

A

Coagulation.

Fibrinolysis.