Part 2-2 (Management of pain and inflammation) Flashcards
Nonopioid Analgesics
NSAIDs
Acetaminophen
NSAIDs primary effects
Analgesic Anti-inflammatory Antipyretic (anti-fever) Anticoagulant Anticancer?
OTC NSAIDs
Aspirin
Ibuprofen
Naproxen
Ketoprofen
Prescription NSAIDs
Etodolac Fenoprofen Ketorolac Meclofenamate Piroxicam
NSAIDs mechanism of action
Inhibit synthesis of prostaglandins
Decrease prostaglandins by inhibiting cyclooxygenase
Prostaglandins
Lipid compounds produced in cells that cause pain, fever, inflammation, and coagulation
COX-1
Normal
Synthesize PGs to protect cells, maintain function
Stomach, kidneys, platelets
COX-2
Induced when cell is injured
Synthesizes PGs that mediate pain, inflammation
RA, other pathologies
COX-2 selective drugs
Inhibit synthesis of PGs in pain, inflammation
Spare production of beneficial PGs in organs
May decrease pain and inflammation w/ less toxicity
Example: Celecoxib
Cox-2 inhibition CV problems
Evidence that COX-2 inhibitors promote infarction
Some drugs recalled
Some NSAIDs more selective for COX-2
COX-2 selective NSAIDs
Diclofenac
Etodolac
Meloxicam
Why does COX-2 inhibition promote infarction
Drugs inhibit dilating PGs; allow PGs that increase platelet activity & promote constriction to dominate
Acetaminophen
Analgesic and antipyretic effects
No gastric irritation
No anti-inflammatory or anticoagulant effects
Liver toxicity high doses
Nonopioids adverse effects
Gastric irritation Hepatic renal toxicity CV problems Impaired bone & cartilage Aspirin toxication
Anti inflammatory steroids
Glucocorticoids
Act on inflammatory cells (macrophages, leukocytes)
Drug-receptor travels to nucleus