inflammation 3 Flashcards

1
Q

chemical mediators of inflammation

A

cell derived mediators
vasocactive amines-histamine and seratoin
acrachidonic acid metabolites
nitric oxide (NO)
cytokines
plasma derived mediators
complement system

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2
Q

histamine

A

present in a PREFORMED state in mast cells, basophils and platelets in cytoplasmic granules-can be released instantly as needed and mast cells typically are found in connective tissue near blood vessels
histamine is released (Degranulation) in response to-physical injury, immune reaction and presence of complement fragments C3a and C5a

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3
Q

action of histamine

A

dilatation of arterioles
increased vascular permeability of venule
causes endothelial contraction in venules

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4
Q

seratonin

A

also known as 5-hydroxytrptamine
preformed in platelets-released in response to platelet aggregation
actions are similar to histamine in acute inflammation

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5
Q

arachidonic acid metabolites

A

degradation of cell membrane phospholipids by phospholipases yields AA

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6
Q

eicosanoids

A

product of aa metabolism
regulate inflammation and gemostasis

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7
Q

two primary classes of inflammatory metabolites

A

prostaglandins
leukotrienes

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8
Q

arachidonic acid metabolites

A

corticosteroids inhibit the action of phospholipases and the production of AA

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9
Q

prostaglandins are produced by cyclooxygenases

A

cox-1 constitutively expressed
cox-2 inducible
include PGE2, PGD2, PGF2a, PGI2 (prostacyclin and TXA (thromboxane)

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10
Q

aspirin and NSAID

A

inhibit cyclooxygenases (cox1 and cox2) and inhibit synthesis of prostaglandins-cox2 selective inhibitor
the activity of lipoxygenases is not affected by NSAID

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11
Q

lipoxygenase pathway

A

lipoxygenase-enzyme that produces leukotrienes and lipoxin from AA
leukotrienes-chemotactic for leukocytes
vascular effects: vasocontraction and increase vascular permeability
lipoxin-lipoxin inhibit inflammation-inhibit leukocyte recruitment and cellular components of inflammation

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12
Q

nitric oxide

A

produced by endothelial cells, macrophages neurons
synthesized by nitric oxide synthase

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13
Q

Nitric oxide two functions in inflammation

A

vasodilation (contributes to vascular reaction)
inhibits cellular inflammatory response-reduces platelet aggregation and adhesion (Anti-inflammatory)
inhibit leukocyte recruitment (anti-inflammatory)
as a free radical kills microbes

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14
Q

cytokine mediators

A

cytokines-polypeptides produce primarily by macrophages and lymphocytes
primary action is modulation of activities of other cells
the main cytokines involved in acute inflammation are IL-1 and TNF (tumor necrosis factor)

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15
Q

plasma protein mediators

A

complement-defense against microbes-formation of MAC (membrane attack complex)
complement activation causes-increase vascular permeability, chemotaxis, opsonization
main components are present as inactive plasma precursors (C1-9)

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16
Q

activation of complement

A

classical pathway
alternative pathway
lectin pathway

17
Q

classical pathway

A

reaction with IgG or IgM containing antigen-antibody complex

18
Q

alternative pathway

A

contact with microbial surfaces and polysaccharides

19
Q

lectin pathway

A

plasma mannose-binding lectin binds to microbes

20
Q

plasma proteases-complement

A

the initial steps in complement activation leads to formation of an enzyme-C3 convertase wich cleaves C3

21
Q

C3 cleavage leads to

A

release of C3a (Anaphylatoxin)
covalent attachment of C3b (initiates formation of C5 convertase)
formation of C5-9 MAC

22
Q

complement derived mediators (formed during cleavage)

A

C3a and C5a-failitate histamine release from mast cells (Vasodilate, increase permeability-aka anaphylatoxin

23
Q

C5a

A

activates lipoxygenase pathway of AA metabolism in neutrophil and monocytes
chemotactic for neutrophils, monocytes eosinophils and basophils