Paracetamol tablets

Non-steroidal Anti-inflammatory drugs (NSADs)

Non-steroidal Anti-inflammatory drugs (NSADs)

Inflammation is a normal, protective response to tissue injury caused by physical trauma, noxious chemicals, or microbiologic agents. Inflammation is the body’s effort to inactivate or destroy invading organisms, remove irritants, and set the stage for tissue repair. Analgesic drugs relieve pain without causing loss of consciousness. The NSAIDs are a group of chemically dissimilar agents that differ in their antipyretic, analgesic, and anti inflammatory activities. 

Role of prostaglandins in pain

The NSAIDs act by inhibiting the synthesis of prostaglandins. Thus, an understanding of NSAIDs requires comprehension of the actions and biosynthesis of prostaglandins. 


Synthesis of prostaglandins

There are two major pathways in the synthesis of the eicosanoids from arachidonic acid, the cyclooxygenase(enzyme) and the lipoxygenase(enzyme)pathways

Therapeutic uses of prostaglandins

Prostaglandins have a major role in modulating pain, inflammation, and fever. They also control many physiological functions, such as acid secretion and mucus production in the gastrointestinal (GI) tract, uterine contractions, and renal blood flow.

Mechanism of action—inactivate cyclo-oxygenases, enzymes required for the production of prostaglandins. 

ASA and traditional NSAIDs inhibit both COX 1 and COX 2

COX 1 is present in all tissues esp. GI, kidneys, endothelial cells and in platelets while COX 2 is Found in brain, bone, kidneys, GI tract, and the female reproductive system Overall, prostaglandins produced by COX 2 are associated with pain and inflammation. Prostaglandins important in:
1.   Protection of kidneys and stomach
2.   Regulate vascular tone and platelets in CV system


Equal in effectiveness to ASA in analgesic and antipyretic effects. Ethanol induces drug-metabolizing enzymes in liver. Resulting rapid metabolism of acetaminophen produces enough toxic metabolite to exceed glutathione. Need glutathione to inactivate toxic metabolites. 

Acetaminophen Poisoning

Toxicity occurs with 20g or more. Creates toxic metabolite that is inactivated by glutathione. Over Dose supply of acetaminophen cause glutathione depletion, hence toxic metabolite are produced which damages liver cells. Not to exceed 4g/day

Treatment of overdose—gastric lavage, Activated charcoal, antidote is Mucomyst (acetylcysteine). Provides cysteine, a precursor to glutathione.



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