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2.1 Acute Inflammation (Acute inflammation (Mediators of acute…
2.1 Acute Inflammation
Acute inflammation
neutrophils leaving the vessels
treat the infection
clear debris from tissue necrosis
edema
causes the swelling
Mediators of acute inflammation
Toll like receptors
PAMP
patterns of molecules on pathogens
let's the body know there is an invader
activation equals
NF-kB activation
turns on acute inflammatory response
Arachicdonic acid
COX
prostaglandins
PGI, PGD, PGE
vasodilation and vascular permeability
Fever and pain
LOX
LTB4
neutrophils
C,D,E4
smooth muscle contraction
bronchospasm
increased vascular permeability
vasoconstriction
mast cells
activated by
tissue trauma
C3a, C5a
cross-linking of cell surface IgE
immediate response
histamine granules
vasodilation
increased vascular permeability
delayed response
leukotrienes
complement
classical pathway
alternative pathway
mannose binding lectin pathway
result
C3 convertase
C5 convertase
MAC
Hageman factor
proinflammatory protein
activated by subendothelial or tissue collagen
coagulation and fibrinolytic systems
DIC
complement
kinin system
HWMK to bradykin
same thing as histamine but inaddition mediate pain
Chronic inflammation
lymphocytes leaving the vessels