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Infla Flashcards

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1
Q

What are the two reasons that suggested the existence of mediators in inflammation?

A
  • Inflammatory changes are uniform across different injuries
  • Inflammation occurs in tissues without nervous connections.
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2
Q

Who described the ‘triple response’ and in what year?

A

Sir Thomas Lewis in 1927

The ‘triple response’ refers to three observable changes in the skin when stroked.

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3
Q

What are the three changes observed in the ‘triple response’?

A
  • Dull red line (erythema)
  • Bright red halo (flare)
  • Swelling (weal).
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4
Q

What causes erythema according to Lewis’s postulation?

A

Release of a humoral histamine-like substance (H-substance)

Erythema is brought about by vasodilation.

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5
Q

What is the role of increased vascular permeability in the ‘triple response’?

A

It causes the swelling (weal)

The weal appears as a result of increased vascular permeability.

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6
Q

What was the significance of Lewis’s experiments?

A

They suggested the action of chemical mediators in inflammation.

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7
Q

What are the two origins of mediators in inflammation?

A
  • Cell-derived
  • Plasma-derived.
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8
Q

What are the two types of cell-derived mediators?

A
  • Preformed (e.g., histamine in mast cells)
  • Newly synthesized (e.g., prostaglandins).
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9
Q

What forms do plasma-derived mediators exist in before activation?

A

Inactive or precursor forms.

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10
Q

What is the principal mediator of the immediate phase of increased vascular permeability?

A

Histamine

Histamine is widely distributed in tissues and stored mainly in the granules of mast cells.

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11
Q

Where is histamine primarily stored?

A

In the granules of mast cells

It is also found in circulating basophils and platelets.

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12
Q

What receptors does histamine act on in venules?

A

H1 receptors

H1 receptors mediate the effects of histamine on vascular permeability.

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13
Q

Histamine is formed from which amino acid?

A

Histidine

The conversion is catalyzed by the enzyme histidine decarboxylase.

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14
Q

Name one type of stimulus that can cause the release of preformed histamine from mast cells.

A

Physical injury

Other stimuli include immune reactions, anaphylatoxins, histamine-releasing proteins, certain cytokines, and neuropeptides.

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15
Q

What happens to the histamine content of the exudate after one hour?

A

It falls

Antihistamines have no effect on delayed permeability responses.

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16
Q

What is the second preformed vasoactive amine mentioned?

A

5-Hydroxytryptamine (5-HT, Serotonin)

5-HT mediates the immediate phase of increased vascular permeability.

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17
Q

In which animals is 5-HT primarily found in mast cells?

A

Rat and mouse

Its presence in chicken mast cells is suspected but not confirmed.

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18
Q

True or False: The role of 5-HT as an inflammatory mediator in animals and humans is established.

A

False

The role of 5-HT in inflammation is not established.

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19
Q

What are arachidonic acid metabolites?

A

Products derived from the metabolism of arachidonic acid that affect inflammation

Includes prostaglandins, leukotrienes, and lipoxins

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20
Q

How do arachidonic acid metabolites act in the body?

A

They act locally at the site of formation and decay either spontaneously or are destroyed enzymatically

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21
Q

What is arachidonic acid?

A

A 20-carbon polyunsaturated fatty acid derived primarily from dietary linoleic acid

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22
Q

In what form does arachidonic acid primarily occur in the body?

A

In its esterified form as a component of cell membrane phospholipids

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23
Q

How is arachidonic acid released from membrane phospholipids?

A

Through the activation of cellular phospholipases by mechanical, chemical, or physical stimuli

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24
Q

What are the two major classes of enzymes involved in arachidonic acid metabolism?

A
  • Cyclooxygenases
  • Lipoxygenases
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25
What do cyclooxygenases synthesize?
Prostaglandins and thromboxanes
26
What do lipoxygenases synthesize?
Leukotrienes and lipoxins
27
What role do arachidonic acid metabolites play in inflammation?
They can mediate virtually every step of inflammation
28
Where is the synthesis of arachidonic acid metabolites increased?
At sites of inflammatory response
29
What effect do agents that inhibit the synthesis of arachidonic acid metabolites have?
They also reduce inflammation
30
What does the cyclooxygenase pathway transform arachidonic acid into?
Prostaglandin endoperoxide
31
What is PGH2 and why is it significant?
PGH2 is highly unstable and is converted enzymatically into three products
32
What is thromboxane A2 and where is it found?
A platelet-aggregating agent and vasoconstrictor found in platelets
33
What enzyme is necessary for the synthesis of thromboxane A2?
Thromboxane synthase
34
Fill in the blank: Arachidonic acid is derived primarily from dietary _______.
linoleic acid
35
True or False: Arachidonic acid occurs freely in the body.
False
36
What is prostacyclin and where is it formed?
Prostacyclin is formed in vascular tissue endothelium, which contains the enzyme prostacyclin synthase.
37
What role does prostacyclin (PGI) play in the body?
PGI is a vasodilator and an inhibitor of platelet aggregation.
38
What is the relationship between thromboxane (TXA) and prostacyclin (PGI) in hemostasis?
TXA and PGI have opposing roles in hemostasis.
39
Which prostaglandins are more stable and formed in many cells?
PGE, PGD, and PGF-alpha.
40
What is the major AA metabolite in mast cells?
PGD.
41
What effects do PGD, PGE, and PGF-alpha have?
They cause vasodilation and potentiate edema formation.
42
How are prostaglandins involved in inflammation?
They are involved in the pathogenesis of pain and fever.
43
What effect does PGE have on pain sensitivity?
PGE increases pain sensitivity to various stimuli.
44
What medications inhibit the synthesis of cyclooxygenase?
Aspirin, indomethacin, and ibuprofen.
45
What enzyme converts arachidonic acid into hydroperoxy derivatives?
5-lipoxygenase.
46
What is 5-HPETE and what happens to it?
5-HPETE is a hydroperoxy derivative of arachidonic acid; it can be reduced to 5-HETE or converted into leukotrienes.
47
What are leukotrienes and how were they named?
Leukotrienes are compounds isolated from leukocytes that contain a triene chain.
48
What is the first leukotriene produced from 5-HPETE?
Leukotriene A4 (LTA4).
49
What does leukotriene B4 (LTB4) do?
LTB4 is a potent chemotactic agent and causes aggregation of neutrophils.
50
What effects do LTC4, LTD4, and LTE4 have?
They cause vasoconstriction, bronchospasm, and increased vascular permeability.
51
True or False: Lipoxins are formed solely by platelets.
False.
52
How are lipoxins synthesized?
Lipoxins are synthesized by transcellular pathways involving cell-cell interaction.
53
What role do neutrophils play in lipoxin formation?
Neutrophils provide LTA4, which platelets convert into lipoxins.
54
What is the relationship between lipoxins and leukotrienes?
There is an inverse relationship; lipoxins may be natural negative regulators of leukotriene actions.
55
What are the actions of lipoxins?
Lipoxins have both pro- and anti-inflammatory actions.
56
Fill in the blank: Lipoxins A4 and B4 are produced from _______.
LTA4.
57
What do the lysosomal granules of neutrophils and monocytes contain that mediates acute inflammation?
Molecules that can mediate acute inflammation ## Footnote These molecules may be released after cell death, by leakage during phagocytic vacuole formation, or by frustrated phagocytosis.
58
What are the two main types of granules found in neutrophils?
Specific (or secondary) granules and azurophil (or primary) granules
59
What do specific granules contain?
* Lysozyme * Collagenase * Alkaline phosphatase * Lactoferrin * Plasminogen activator * Histaminase
60
What do azurophil granules contain?
* Myeloperoxidase * Bactericidal factors (lysozyme, defensins) * Acid hydrolases * Neutral proteases (elastase, cathepsin G, non-specific collagenases, proteinase 3)
61
What is the role of acid proteases in neutrophils?
Degrade bacteria at an acid pH within the phagolysosomes
62
What do neutral proteases degrade?
* Extracellular components * Elastin * Collagen * Basement membrane * Other matrix proteins
63
How can unchecked leukocyte infiltration affect tissue?
Can lead to increased vascular permeability, chemotaxis, and tissue damage
64
What is the major inhibitor of neutrophil elastase?
Alpha-I-antitrypsin
65
What is Platelet Activating Factor (PAF)?
A phospholipid-derived mediator that aggregates platelets and causes degranulation
66
How is PAF generated?
From membrane phospholipids of various cell types by the action of phospholipase A2
67
What are the effects of PAF?
* Vasoconstriction * Vasodilation (at low concentrations) * Increased vascular permeability * Increased leukocyte adhesion * Chemotaxis * Degranulation * Oxidative burst
68
What are oxygen-derived free radicals, and from where are they released?
Released extracellularly from neutrophils and macrophages after exposure to various agents
69
What are the major species of reactive oxygen produced within neutrophils?
* Superoxide (O2') * Hydrogen peroxide (H2O2) * Hydroxyl radical (OH')
70
What is the role of nitric oxide (NO) in inflammation?
* Vasodilator * Reduces platelet and leukocyte adhesion * Acts as a microbicidal agent in activated macrophages
71
What enzyme synthesizes nitric oxide (NO)?
Nitric oxide synthase (NOS)
72
What are the three types of nitric oxide synthase (NOS)?
* Type I (nNOS) * Type II (eNOS) * Type III (iNOS)
73
What is the function of Type I (nNOS)?
Constitutively expressed neuronal NOS present in neurons
74
What is the function of Type II (eNOS)?
Constitutively synthesized NOS found mainly within endothelium
75
What induces Type III (iNOS)?
Activated by cytokines (TNF-alpha, IFN-gamma) or other agents
76
What is the chemical composition of Platelet Activating Factor (PAF)?
Acetyl glycerol ether phosphocholine (AGEPC)

Inflammation (1 decks)

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