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Some textbooks put these drugs after the opiate analgesics and others group the antiarthritis drugs together. Basically, we will consider here some salient features of the nonnarcotic analgesics and some of the anti-inflammatory agents. I’ve also included the drugs used for gout and migraines. The largest group of drugs here is the nonsteroidal anti-inflammatory drugs (NSAIDs). This group includes aspirin and salicylates. However, the salicylates and aspirin have some important special features, so I have separated them to emphasize these features.


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IBUPROFEN meclofenamate
KETOROLAC oxaprozin
NAPROXEN phenylbutazone
diclofenac piroxicam
etodolac sulindac
fenoprofen suprofen
flurbiprofen tolmetin
mefenamic acid  

Compare this list with the one in your textbook or class handouts. There seems to be no rhyme or reason to the names.

All the nonsteroidal anti-inflammatory drugs (NSAIDs) (including aspirin) are thought to exert their clinical effects by inhibiting prostaglandin synthesis.

The primary site of action is the cyclooxygenase (COX) enzyme, which catalyzes the conversion of arachidonic acid to prostaglandin and endoperoxide (Figure 45–1). Prostaglandins modulate components of inflammation. They also are involved in control of body temperature, pain transmission, platelet aggregation, and other effects. They are not stored by cells but are synthesized and released on demand. Their half-lives are only minutes long. Therefore, if you control the enzyme that makes prostaglandins, you control the prostaglandins themselves.


Remember that arachidonic acid is converted to both prostaglandins and leukotrienes. The nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the enzyme cyclooxygenase and, therefore, the formation of prostaglandins.

All the NSAIDs (including aspirin) have analgesic, antipyretic, and anti-inflammatory effects. The older (nonspecific) NSAIDs also have antithrombotic effects.

The NSAIDs (including aspirin) are used in the treatment of moderate pain, fever, tendinitis, sunburn, rheumatoid arthritis, and osteoarthritis, just to name a few.

The most common adverse effects of the NSAIDs (including aspirin) are gastrointestinal (GI) injury and renal injury.

Gastrointestinal (GI) injury consists of gastritis and ulcers. Misoprostol, a synthetic prostaglandin analogue, is used for the prevention of NSAID-induced ulcers. NSAIDs can cause oliguria, fluid retention, decreased sodium excretion, renal failure, and can prolong bleeding time.

The agents differ with respect to their central nervous system (CNS) side effects, duration of action, degree of platelet antagonism (bleeding), and GI toxicity.

KETOROLAC is an NSAID that can be administered intramuscularly or intravenously. Ibuprofen and meloxicam are now also available for intravenous administration.


Two isoforms of the COX enzyme have been identified. COX-1 is expressed constitutively in most tissues and is thought to protect the gastric ...

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