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DWT > Pathology 8: Chemical Mediators of Inflammation > Flashcards

Pathology 8: Chemical Mediators of Inflammation Flashcards

1
Q

What are the types of cell derived mediators?

A
  • Vasoactive amines: histamine and serotonin
  • Arachondonic acid metabolites
  • Nitric oxide (NO)
  • Cytokines
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2
Q

What are the types of plasma derived mediators?

A

Complement system

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3
Q

Where is histamine stores?

A

In a performed state in
- mast cells
- basophils
- Platelets

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4
Q

How quickly can histamine be released if needed?

A

Instantly

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5
Q

Where are mast cells normally located?

A

In connective tissues near BV
- may release histamine

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6
Q

What is histamine released in response to?

A
  • Physical injury (heat, cold, trauma)
  • Immune rxn (IgE binding)
  • Presence of complement fragments C3a and C5a (anaphylatoxins)
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7
Q

What are the actions of histamine?

A
  • Dilation of arterioles
  • Increased vascular permeability of venules
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8
Q

what does Increased vascular permeability of venules lead to?

A

endothelial contraction in venules

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9
Q

What is 5-hydrooxytryptamine?

A

Serotonin

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10
Q

Where is serotonin stored preformed? and what is it released in response to?

A
  • Platelets
  • Platelet aggregation
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11
Q

What is the action of serotonin?

A
  • Dilation of arterioles
  • Increased vascular permeability of venules

** Same as histamine

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12
Q

Where does arachidonic acid come from?

A

The degradation of phospholipids by phospholipase

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13
Q

What is eicosanoids?

A

Products of arachidonic acid metabolism

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14
Q

What is special about eicosanoids?

A

it regulates inflammation and homeostasis

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15
Q

What are the two primary classes of inflammatory metabolites?

A
  • Prostaglandins and leukotrienes
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16
Q

What do corticosteroids inhibit?

A

The action of phospholipases and therefore any production at all of arachidonic acid

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17
Q

What are prostaglandins produced by?

A

Cyclooxygenases
- COX-1: always expressed
- COX-2: inducible

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18
Q

What are the prostaglandins?

A

Prostacyclins:
- PGE2
- PGI2
- PGF2
- PGD2
Thromboxane:
- TXA2

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19
Q

What do asprin and NSAIDS inhibit?

A

COX-1 and COX-2 therefore inhibiting of prostaglandins

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20
Q

What is unaffected by NSAIDS?

A

lipoxygenase

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21
Q

What is lipoxygenase?

A

An enzyme that produces leukotrienes and lipoxins from arachidonic acid

22
Q

What is leukotrienes actions?

A
  • Chemotaxis for leukocytes
  • Vascular effects: vasoconstriction and increased vascular permeability
23
Q

What do lipoxins inhibit?

A
  • Inflammation
  • Inhibit leukocyte recruitment and cellular components of inflammation
24
Q

What produces Nitric Oxide?

A

-Endothelial cells
-Macrophages
- Neurons

25
Q

What is nitric oxide synthesized by?

A

Nitric oxide synthase

26
Q

What is nitric oxide function in inflammation?

A
  • Vasodilation
  • Inhibits cellular inflammatory response
27
Q

How does nitric oxide inhibits cellular inflammatory response?

A
  • Reduces platelet aggregation and adhesion (anti-inflammatory)
  • Inhibits leukocyte recruitment
28
Q

In what form does Nitric oxide kill microbes?

A

As free radicals

29
Q

What are cytokines?

A

polypeptides produced primarly by macrophages and lymphocytes

30
Q

What is the action of cytokines?

A

Modulation of activities of other cells

31
Q

What are the main cytokines involved in acute inflammation?

A
  • IL-1
  • TNF (tumor necrosis factor)
32
Q

What are the actions of IL-1 and TNF on vascular endothelium?

A
  • Inc expression of leukocytes adhesion molecules
  • Production of IL-1 and chemokines
  • Increase in pro-coagulation and decrease in anticoagulation activity
33
Q

What are the actions of IL-1 and TNF on leukocytes?

A
  • activation
  • production of cytokines
34
Q

What are the actions of IL-1 and TNF on fibroblasts?

A
  • Proliferation
  • Increase in collagen synthesis
35
Q

What are the systemic affects of IL-1 and TNF?

A
  • Fever
  • Leukocytosis
  • Increased acute-phase proteins
  • Decreased appetite
  • Increase sleep
36
Q

What is a complement plasma protein mediator?

A
  • Defense system against microbes
  • Formation of MAC- membrane attack complex
37
Q

What does compliment activation cause?

A
  • increased vascular permeability
  • Chemotaxis
  • Opsonization
38
Q

What are complement proteins stored as?

A

Inactive plasma precursors: C1-9

39
Q

What are the three pathways of complement activation?

A
  • Classical
  • Alternative
  • Lectin
40
Q

What is the classical pathway of complement activation?

A
  • Reaction with IgG and IgM containing antigen-antibody complex
41
Q

What is the alternative pathway of complement activation?

A
  • Contact with microbial surfaces and polysaccharides
  • Ex: cobra venom and endotoxins
42
Q

What is the lectin pathway of complement activation?

A

Plasma mannose-binding lectin binds to microbes

43
Q

What does complement activation lead to?

A

Formation of enzyme C3 convertase

44
Q

What does C3 convertase do?

A

Cleaves C3

45
Q

what does C3 cleavage lead to?

A
  • Release of C3a (anaphylatoxin)
  • Covalent attachment of C3b (initiates formation of C5 convertase)
46
Q

What does C5 convertase lead to?

A

Formation of C5-9 (MAC)

47
Q

What are the complement derived mediators?

A
  • C3a
  • C5a
  • C3b
48
Q

What are the anaphylatoxins?

A
  • C3a and C5a
49
Q

What does C3a and C5a do?

A

Facilitate histamine release from mast cell
- Vasodilate
- Increase permeability

50
Q

What does just C5a do?

A
  • Activates lipoxygenase pathway of arachidonic acid metabolism in neutrophils and monocytes
  • Chemotactic for neutrophils, monocytes, eosinophils, and basophils
51
Q

What does c3b do?

A

Acts as opsonins when fixed to bacteria; facilitating phagocytosis by neutrophils and macrophages (receptor)

DWT (28 decks)

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