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NSAIDs

Steroid - Block Phospholipase A2 enzyme

NSAIDs - Block COX enzyme (indirectly block formation of prostaglandins)

Mechanism of action
COX-I Inhibition - Unwanted effects on GIT & kidney
- ↓ Platelet aggregation
COX-II Inhibition - Anti inflammatory
- Analgesic
- Antipyretic
NSAIDs

Classification Types Examples MOA Actions Side Effects

Nonselective Propionic acid derivatives Ibuprofen Oral administration Anti-inflammatory
COX inhibitors Metabolised in liver
Excreted in kidney
Indole derivatives Indomethacin Not recommended as analgesic or Rheumatoid arthritis GIT symptoms (ulceration,
antipyretic (severe side-effects) Ankylosing spondylitis nausea, abdominal pain,
Gout headaches)
Oxicam derivatives Piroxicam Excreted in kidney (parent drug and Rheumatoid arthritis GIT disturbances (Piroxicam)
Meloxicam metabolites) Ankylosing spondylitis
Osteoarthritis
Salicylates Aspirin Irreversibly inhibits COX-1 Antiplatelet GIT (gastric & intestinal mucosal
(Other NSAIDs – reversible inhibitors of Antipyretic damage, erosions, peptic ulcer,
COX) Analgesic GIT hemorrhage, indigestion,
Prevents formation of products Anti-inflammatory (↑ dose) gastro-oesophageal reflux)
(thrombaxane, prostacycline,
prostaglandins) ↑ GIT bleeding – inhibit
Oral or rectal administration prostaglandin (PG) synthesis
Excreted in kidney (PG – inhibit acid secretion,
promote secretion of mucus)

Renal (↓ renal blood flow,

hypertension, GFR ↓)

Salicylism
Allergy
Reye’s syndrome
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Selective COX-II Celecoxib Block production of prostaglandins Analgesic ↑ heart attack risk
Inhibitors Rofecoxib (without interfering gastric protection Anti-inflammatory
Valdecoxib or platelet activity) Headache, dyspepsia, diarrhoea,
Metabolised in liver abdominal pain (Celecoxib)
Excreted in feces and urine

Drug MOA Actions Side effects

Acetaminophen (Paracetamol)
Inhibit prostaglandin synthesis in CNS
(COX-3)
Oral or rectal administration
Safe in pregnancy & breast feeding
Metabolised in liver
Analgesic Hepatotoxicity (5g/day)
Antipyretic
Not NSAID (no anti-inflammatory & Mechanism of toxicity
antiplatelet effects) 1. After phase 1 metabolism, NAPQI
formed (N-acetyl-p-
benzoquinoneimine) (toxic
metabolite)
2. NAPQI inactivated by glutathione
3. In ↑ [NAPQI ], insufficient
glutathione available
4. NAPQI react with cellular membrane
(hepatocyte damage & death)

In case of paracetamol overdose

1. ↑ glutathione in liver (methionine,
N-acetylcysteine)