Anti-Inflammatory Agents Flashcards
3 phases of inflammation
acute inflammation
immune response
chronic inflammation
Mediators released in acute inflammation
histamine serotonin bradykinin prostaglandins leukotrienes
Chronic inflammation causes
pain
destruction of tissue
disability
Acute inflammation precedes
immune response
2 pathways of mediator synthesis
cyclooxygenase
lipoxygenase
Prostaglandins are
proinflammatory mediators
Cyclooxygenase mediators
COX 1 & COX 2:
prostaglandins
prostacyclins
Thromboxane A2
Lipoxygenase pathway mediators
Leukotrienes
E cosanoids (4) that cause vasoconstriction, bronchospasm and increased permeability
Leukotriene A4
Leukotriene C4
Leukotriene D4
Leukotriene E4
steroids inhibit
phospholipases
12-Lypoxygenase —>
Lypoxin A4
Lypoxin B4
Lypoxin effects
Vasodilation
inhibit neutrophil chemotaxis
stimulate monocyte adhesion
Prostaglandin PGI2 effect
vasodilation
inhibits platelet aggregation
Thromboxane A2 effect
vasoconstriction
promotes platelet aggregation
COX 1 & COX 2 inhibitors inhibit
cyclooxygenase
Prostaglandin G2 —>
Prostaglandin PGI2
Thromboxane A2
PGE2
PGE2 effects
vasodilation
potential edema
NSAIDs block what pathway?
Prostaglandin G2
Steroids block
the entire inflammation cascade
Steroids are superior/in-superior?
superior
Steroids’ side effects are
more systemic
Effect of E cosanoids on vascular muscle
vasodilation or vasoconstriction
Effect of E cosanoids on GI muscle
contraction, colic
Effect of E cosanoids on uterus
contraction
Effect of E cosanoids on pulmonary muscle
constriction
activity of NSAIDs is mediated by inhibition of
prostaglandins
(NSAIDs) inflammation is reduced by
decreasing the release of mediators from granulocytes, basophils and mast cells
NSAID effects
analgesic
anti-inflammatory
antipyretic
inhibit platelet aggregation
NSAIDS irritate
the GI tract