NSAIDs Flashcards
(42 cards)
Inflammation
Active response of tissues to injury (beneficial or harmful)
Processes involved in inflammation
Immune responses, coagulation cascade, regeneration and repair
4 changes involved in inflammation
Vasodilation, edema, WBCs enter tissue, pain
Fibrosis
Scarring as a result of chronic inflammation
Inciting causes of inflammation
Infection, trauma, necrosis, immune-mediated disease
Beneficial outcomes of inflammation
Eliminates agent, repairs + regenerates
Harmful outcomes of inflammation
Loss of function, systemic effects, scar formation
Synthesis of inflammatory mediators
Some synthesized in advance (histamine), some synthesized at the site (prostaglandins)
Redundancy of inflammatory mediators
Many trigger the same response
Major classes of pro-inflammatory mediators
Eicosanoids (prostaglandins, thromboxane, prostacyclin), leukotrienes
Non-pharmacological treatments of inflammation
Rest, heat/cold, weight reduction, surgery
Pharmacological treatments of inflammation
NSAIDs, glucocorticoids
Oldest NSAID
Aspirin
Mechanism of aspirin
Inhibits prostaglandin synthesis
Main benefits of NSAIDs
Anti-inflammatory, antipyretic, analgesic
Normal physiological roles of prostaglandins
Synthesized from arachidonic acid by COX enzymes
COX1
Housekeeping enzyme at lowlevels in all tissues; produces thromboxane, other prostaglandins, prostacyclins
COX2
Normally present at very low levels in most tissues, very important for homeostasis in some tissues
TXA2
Thromboxane, important for platelet aggregation
PGD2, PGE2
Prostaglandins synthesized by both cox enzymes; maintain blood flow and are involved in gastric mucosa protection
PGI2
Prostacyclin; inhibit platelet aggregation, vasodilate, and protect gastric mucosa
Prostaglandin roles during inflammation
COX2 is upregulated locally, causing the 5 main symptoms of inflammation
NSAIDs mechanism
Inhibit usually both COX1 and COX2
Major benefit of NSAIDs
Reduces blood flow to the site of injury