Nonsteroidal anti-inflammatory drugs (NSAIDs) are used primarily to treat inflammation, mild-to-moderate pain, and fever.
Analgesics, Antipyretics, and NSAIDs
Nonsteroidal
anti-inflammatory drugs (NSAIDs) are used primarily to treat inflammation,
mild-to-moderate pain, and fever. Specific uses include the treatment of
headache, arthritis, sports injuries, and menstrual cramps. Aspirin is used to
inhibit the clotting of blood and prevent strokes and heart attacks in
individuals at high risk. NSAIDs are also included in many cold and allergic
preparations.
NSAIDs are
associated with a number of side effects. The frequency of side effects varies
according to the drugs; the most common side effects are gastro intestinal
tract (GIT) disturbances, such as nausea, diarrhoea, constipation, vomiting,
decreased appetite, and peptic ulcer. NSAIDs may also cause fluid retention,
leading to oedema; the most serious side effects are kidney failure, liver
failure, ulcers, and prolonged bleeding after an injury of surgery. Some
individuals are allergic to NSAIDs and may develop shortness of breath when
NSAIDs are administered. People with asthma are at a higher risk for
experiencing serious allergic reaction to NSAIDs. Use of aspirin in children
and teenagers with chicken pox or influenza has been associated with the
development of Reye’s syndrome. Therefore, aspirin and salicylate should not be
used in children and teenagers with suspected or confirmed chicken pox or
influenza.
Antipyretics
are the drugs that reduce the elevated body temperature. Anti-inflammatory
agents are used to cure or prevent inflammation caused by prostaglandin (PGE2).
These drugs are widely utilized for the alleviation of minor aches, pains,
fever, and symptomatic treatment of rheumatic fever, rheumatoid arthritis, and
osteoarthritis. The biosynthetic pathway of prostaglandins (PGs) is depicted in
Figure 3.1
PG is a
naturally occurring 20-carbon cyclopentano fatty acid derivative, derived from
arachidonic acid.
Mode of action: NSAIDs inhibit cycloxygenase (COX), the enzyme that catalyses
the synthesis of cyclic endoperoxides, from the arachidonic acid to form PGs.
The two COX isoenzymes are COX-1 and COX-2. The function of COX-1 is to produce
PGs that are involved in normal cellular activity, (protection of gastric
mucosa, maintenance of kidney function). While, COX-2 is responsible for the
production of PGs at the inflammation sites. Most NSAIDs inhibit both COX-1 and
COX-2 with varying degree of selectivity. Selective COX-2 inhibitor may
eliminate the side effects associated with NSAIDs due to COX-1 inhibition, such
as gastric and renal effect.
In stomach: Biosynthesis of PGs, especially PGE2 and PGI2,
serves as cytoprotective agents in gastric mucosa; these PGs inhibit acid
secretion by the stomach, enhance mucosal blood flow, and promote the secretion
of cytoprotective mucus in the GIT. Inhibition of the PGs synthesis may make
the stomach more susceptible to damage and lead to gastric ulcer.
In platelets: Platelet’s function get disturbed because NSAIDs prevent the
formation of Thromboxane A2 (TXA2) in platelets, as TXA2 is a potent
platelet-aggregating agent. This accounts for the tendency of these drugs to
increase the bleeding time and this side effect has been exploited in the
prophylactic treatment of thromboembolic disorder.
In uterus: NSAIDs prolong gestation because of the inhibition of PGF2 in
uterus. PGF2 is a potent uterotropic agent and their biosynthesis by uterus
increase dramatically in the hours before parturition. Accordingly, some
anti-inflammatory drugs have been used as a colytic agent to inhibit preterm
labour.
In kidney: NSAIDs decrease renal blood flow and the rate of glomerular
filtration in patients with congestive heart failure, hepatic cirrhosis, and
with chronic renal disease, in addition, they prolong the retention of salt and
water, this may cause oedema in some patients.
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