Pharmacology: Pharmacodynamics: Mode or Mechanisms of Action: Mefenamic acid is an analgesic with anti-inflammatory properties, and a demonstrable antipyretic effect.
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the activity of the enzyme cyclo-oxygenase, resulting in decreased formation of precursors of prostaglandins and thromboxanes from arachidonic acid. Although the resultant decrease in prostaglandin synthesis and activity in various tissues may be responsible for many of the therapeutic (and adverse) effects of NSAIDs, other actions may also contribute significantly to the therapeutic effects of these medications.
Analgesic: May block pain impulse generation via a peripheral action that may involve reduction of the activity of prostaglandins, and possibly inhibition of the synthesis or actions of other substances that sensitise pain receptors to mechanical or chemical stimulation.
Antidysmenorrheal: By inhibiting the synthesis and activity of intrauterine prostaglandins (which are thought to be responsible for the pain and other symptoms of primary dysmenorrhea), NSAIDs decrease uterine contractility and uterine pressure, increase uterine perfusion, and relieve ischemic as well as spasmodic pain. Also, NSAIDs may relieve to some extent extrauterine symptoms (such as headache, nausea, and vomiting) that may be associated with excessive prostaglandin production.
Vascular headache prophylactic and suppressant: Analgesic actions may be involved in relief of headache. Also, by reducing prostaglandin activity, NSAIDs may directly prevent or relieve certain types of headache thought to be caused by prostaglandin-induced dilation or constriction of cerebral blood vessels.
Pharmacokinetics: Mefenamic acid is well absorbed after oral administration with peak plasma concentration occurring at 2 - 4 hours. The plasma half-life is around 3 hours. Mefenamic acid is extensively bound to plasma proteins (99%). Over 50% of a dose may be recovered in the urine, as unchanged drug or conjugated metabolites.