Pharmacology of Inflammation Flashcards
increase vascular permeability, bronchoconstriction
leukotrienes
prostaglandins class
lipid mediators
increased extracellularly during injury: anti-inflammatory, inhibit cytokine action
adenosine
glucocorticoids cellular source
adrenal cortex
bradykinin cellular source
endothelial cells
bradykinin class
peptide
Oxygen-derived free radicals class
superoxide, hydroxy radicals
vasodilation, pain, fever, platelet aggregation (via thromboxane)
prostaglandins
cell adhesion molecules mechanism
contact molecules, calcium dependent
prostaglandins mechanism
activation of specific GPCRs
adenosine cellular source
all cells
leukotrienes mechanism
activation of GPCRs
glucocorticoids class
lipid mediators
prostaglandins cellular source
virtually all cells
complement system cellular source
synthesized by liver, circulate in blood
C-reactive protein class
plasma proteins
Histamine cellular source
mast cells, basophils
complement system mechanism
complement protein complexes cause osmotic lysis activation of GPCRs
C-reactive protein cellular source
produced in liver in response to cytokines, also produced in adipocytes
cell adhesion molecules cellular source
endothelial cells, platelets, leukocytes
leukotrienes cellular source
macrophages, neutrophils
cytokines mechanism
bind to specific receptor proteins to induce gene expression of number of proteins via activation of Nf?B and AP-1; increase COX (fever) and lipoxygenases, increase adhesion molecule expression, induce collagenase (fibrosis)
inhibition of cytokines, inhibition of phospholipase A2, inhibition of COX-2, inhibition of cell adhesion molecules
glucocorticoids
vasodilation, increased vascular permeability, pain
histamine