inflammation 3 Flashcards
chemical mediators of inflammation
cell derived mediators
vasocactive amines-histamine and seratoin
acrachidonic acid metabolites
nitric oxide (NO)
cytokines
plasma derived mediators
complement system
histamine
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
action of histamine
dilatation of arterioles
increased vascular permeability of venule
causes endothelial contraction in venules
seratonin
also known as 5-hydroxytrptamine
preformed in platelets-released in response to platelet aggregation
actions are similar to histamine in acute inflammation
arachidonic acid metabolites
degradation of cell membrane phospholipids by phospholipases yields AA
eicosanoids
product of aa metabolism
regulate inflammation and gemostasis
two primary classes of inflammatory metabolites
prostaglandins
leukotrienes
arachidonic acid metabolites
corticosteroids inhibit the action of phospholipases and the production of AA
prostaglandins are produced by cyclooxygenases
cox-1 constitutively expressed
cox-2 inducible
include PGE2, PGD2, PGF2a, PGI2 (prostacyclin and TXA (thromboxane)
aspirin and NSAID
inhibit cyclooxygenases (cox1 and cox2) and inhibit synthesis of prostaglandins-cox2 selective inhibitor
the activity of lipoxygenases is not affected by NSAID
lipoxygenase pathway
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
nitric oxide
produced by endothelial cells, macrophages neurons
synthesized by nitric oxide synthase
Nitric oxide two functions in inflammation
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
cytokine mediators
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)
plasma protein mediators
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)