NSAIDs Flashcards
3 Categories of NSAIDs
Salicylates (Aspirin), Traditional, COX-2 Specific
General Mechanism
NSAIDs competitively inhibit COX enzymes from converting arachidoic acid to PGs (Aspirin irreversible, Necolexin only to COX-2) in order to prevent the prostaglandins and thromboxane in order to stop pain, fever and inflammation from happening.
NSAID Purpose
Pain Relief
Fever Reduction
Reduce Inflammation
Aspirin Purpose
Moderate pain of muscle, joints, headache, dental
Inflammatory diseases like arthritis
Small doses prevent stroke/MI
Pain, Fever, Inflammation
Aspirin Mechanism
Aspirin acetylates the active binding pocket of COX-1 and COX-2 and therefore stopping prostaglnadin formation.
Inhibition of COX-2 is less potent
Aspirin Specific Toxicity
Reye’s Syndrome- Aspirin to a child or adolecent with a fever from a febrile virus can kill them due to encephalitis
Acute Gouty Attack- By preventing the elimination of uric acid in the kidneys
Aspirin and CVD
81 mg/day can act as primary or secondayr prevention of MI/Stroke or treat an occlusive stroke by acetylating COX-1 in platelets to permanently shut down TXA2 formation while maintaining endothelial COX-1 production of PGI2 –> this creates an anti-thrombotic state
Other Salicylates
Less Potent/Less risky NSAIDs than aspirin and better for patients with GI symptoms or bleeding problems
IND- pain, fever or inflammation
Toxicity = salicylate intox and can lead to respiratory depression and death
Traditional NSAIDs
Ibuprofen, naproxen, oxaproxin. indomethacin, diclofenac, keterolac
T-NSAID MEchanisms
Competitively inhibit both COX-1 and COX-2 to stop inflammation, pain and fever
T-NSAID Indications
Moderate pain, arthritis, fever
Ibuprofen
Rapid onset and good for ACUTE pain
Naproxen
Rapid onset and long half life (14 hrs)
Oxaproxin
Long half life (once a day)
Indomethacin
Potent anti-inflammatory
Treat Patent Ductus Arteriosis
Diclofenican
COX-2 selective, high toxicity of MI/Stroke
Ketorolac
IN Anasgleic in post surgery
Good for opioid tolerance/addiction
Adverse Affects
GI, Renal, cardio, platelet, hypersensitivity, CNS, pregnancy
GI
Bleeding, Ulcers, Vomiting due to high acid, low bicarb, low mucus which is all the job of housekeeping Pgs from COX-1
Renal
Hemodynamic Acute Renal Failure
Acute Interstitial Nephritis
Analgesic Nephropathy
Cardio
Exacerbate HTN/HF with vasoconstriction and increased afterload
Platelet
Low TXA2- low clotting- bleeding
Hypersensitivity
Asthmatic like attack due to arachidoic acid going down a different pathway and affecting pulmonary
Pregnancy
Premature closure of ducus arteriosis
Delayed Labor from low PGE2, PGE2Fa
Celecoxib
COX-2 selective
Works the same at COX 2
Toxicity = CVD risks due to low PGI2 and a pro-thrombotic environment
Acetaminophen
Tylenol
Indicated for mild to moderate pain and fever but not peripheral inflammation
AM404 stops COX-2 in brain and acts on canibinoid receptors
Good to avoid adverse effects of NSAIDs
Bad = NAPQI and low glutathione = OD and liver failure
NSAID Interactions
Baby aspirin + NSAID = antagonize
Warfarin + NSAID = high warfarin and bleeding
Anti-HTN + NSAID = vasoconstriction and still HTN
Hypoglycemics + Salicylate = Hypoglycemia
Lithium, Methotextrate or Aminoglycoside and NSAID = renal toxicity
NSAID Contraindications
GI Ulcers,Hemophilia, Renal Disorder, CVD, NSAID Hypersensitivity, Pregnant lady, No aspirin if gout or child with temp (Reye’s)
