{"id":6615,"date":"2024-11-18T12:19:19","date_gmt":"2024-11-18T12:19:19","guid":{"rendered":"https:\/\/workhouse.sweetdishy.com\/?p=6615"},"modified":"2024-11-18T12:19:20","modified_gmt":"2024-11-18T12:19:20","slug":"nsaids-for-special-indications","status":"publish","type":"post","link":"https:\/\/workhouse.sweetdishy.com\/index.php\/2024\/11\/18\/nsaids-for-special-indications\/","title":{"rendered":"NSAIDS FOR SPECIAL INDICATIONS"},"content":{"rendered":"\n

Indomethacin
<\/strong>Indomethacin is slightly more toxic but in certain circumstances more effective than aspirin.
Indomethacin is well absorbed after oral administration and highly bound to plasma proteins.
Metabolism occurs in the liver and unchanged drug and inactive metabolites are excreted in bile
and urine.
Clinical Uses: treatment of patent ductus arteriosus, acute gouty arthritis and ankylosing
spondylitis, pericarditis and pleurisy.
Adverse Effects<\/em>:<\/strong> The gastrointestinal effects may include abdominal pain, diarrhea,
gastrointestinal hemorrhage, and pancreatitis. CNS effects include be associated with dizziness,
confusion, and depression. Serious hematologic reactions’ including thrombocytopenia and
aplastic anemia has been reported.
Acetaminophen<\/strong>
Acetaminophen is the active metabolite of phenacetin responsible for its analgesic effect. It is a
weak prostaglandin inhibitor in peripheral tissues and possesses no significant antiinflammatory effects.
Pharmacokinetics: Acetaminophen is administered orally. Absorption is related to the rate of
gastric emptying. Acetaminophen is slightly bound to plasma proteins and is partially
metabolized by hepatic microsomal enzymes.
Indications: It is an effective analgesic and antipyretic agent, but it lacks of anti-inflammatory
properties. The drug is useful in mild to moderate pain such as headache, myalgia, and
postpartum pain.
Adverse Effects: It is hepatotoxic (contraindicated in patients with known liver diseases), and
also causes hemolytic anemia and methemoglobinemia
DRUGS USED IN GOUT<\/strong>
Gout is a familial metabolic disease characterized by recurrent episodes of acute arthritis due to
deposits of monosodium urate in joints and cartilage. Formation of uric acid calculi in the

kidneys may also occur. Gout is usually associated with high serum levels of uric acid, a poorly
soluble substance that is the major end product of purine metabolism.
The treatment of gout is aimed at relieving the acute gouty attack and preventing recurrent
gouty episodes and urate lithiasis. Urate crystals are initially phagocytosed by synoviocytes,
which then release prostaglandins, lysosomal enzymes, and interleukin-1. Attracted by these
chemotactic mediators, polymorphonuclear leukocytes migrate into the joint space and amplify
the ongoing inflammatory process. In the later phases of the attack, increased numbers of
mononuclear phagocytes (macrophages) appear, ingest the urate crystals, and release more
inflammatory mediators.
Colchicine<\/strong>
Colchicine is absorbed readily after oral administration. Metabolites of the drug are excreted in
the intestinal tract and urine.
Colchicine dramatically relieves the pain and inflammation of gouty arthritis without altering the
metabolism or excretion of urates and without other analgesic effects. Colchicine produces its
anti-inflammatory effects by inhibition of leukocyte migration and phagocytosis. It also inhibits
the formation of leukotriene B4.
Indications: Colchicine is used for alleviating the inflammation of acute gouty arthritis.
Adverse Effects: Colchicine often causes diarrhea and may occasionally cause nausea,
vomiting, and abdominal pain. Colchicine may rarely cause hair loss and bone marrow
depression as well as peripheral neuritis and myopathy. Acute intoxication after ingestion of
large (nontherapeutic) doses of the alkaloid is characterized by burning throat pain, bloody
diarrhea, shock, hematuria, and oliguria.
NSAIDS in Gout<\/strong>
Indomethacin and other NSAIDs inhibit urate crystal phagocytosis. Indomethacin may be used
as initial treatment of gout or as an alternative drug when colchicine is unsuccessful or causes
too much discomfort. Indomethacin is the agent most often used today to treat acute gout. All
other NSAIDs except aspirin can be used to treat acute gouty episodes.
Uricosuric Agents<\/strong>
Probenecid and sulfinpyrazone are uricosuric drugs employed to decrease the body pool of
urate in patients with tophaceous gout or in those with increasingly frequent gouty attacks. In a
patient who excretes large amounts of uric acid, the uricosuric agents should be avoided so as

not to precipitate the formation of uric acid calculi. Uricosuric drugs are organic acids and act at
the anionic transport sites of the renal tubule.
Pharmacokinetics: Probenecid is completely reabsorbed by the renal tubules and is metabolized
very slowly. Sulfinpyrazone or its active hydroxylated derivative is rapidly excreted by the
kidneys. Its effect after oral administration is almost that of probenecid.
Pharmacodynamics: Uric acid is freely filtered at the glomerulus. Like many other weak acids, it
is also both reabsorbed and secreted in the middle segment of the proximal tubule. Uricosuric
drugs probenecid, sulfinpyrazone, and large doses of aspirin affect these active transport sites
so that net reabsorption of uric acid in the proximal tubule is decreased. Because aspirin in
small doses causes net retention of uric acid by inhibiting the secretory transporter, it should not
be used for analgesia in patients with gout.
Indications: Uricosuric therapy should be initiated if several acute attacks of gouty arthritis have
occurred, when evidence of tophi appears, or when plasma levels of uric acid in patients with
gout are so high that tissue damage is almost inevitable.
Adverse Effects: Both drugs cause gastrointestinal irritation, but sulfinpyrazone is more active in
this regard. Probenecid is more likely to cause allergic dermatitis, but a rash may appear after
the use of either compound. Nephrotic syndrome has resulted from the use of probenecid. Both
sulfinpyrazone and probenecid may cause aplastic anemia.
Allopurinol<\/strong>
An alternative to increasing uric acid excretion in the treatment of gout is to reduce its synthesis
by inhibiting xanthine oxidase with allopurinol.
Allopurinol is absorbed after oral administration. Like uric acid, allopurinol is itself metabolized
by xanthine oxidase. The resulting compound, alloxanthine, retains the capacity to inhibit
xanthine oxidase and has a long duration of action.
Pharmacodynamics: Dietary purines are not an important source of uric acid. The quantitatively
important amounts of purine are formed from amino acids, formate, and carbon dioxide in the
body. Those purine ribonucleotides not incorporated into nucleic acids and those derived from
the degradation of nucleic acids are converted to xanthine or hypoxanthine and oxidized to uric
acid. When this last step is inhibited by allopurinol, there is a fall in the plasma urate level and a
decrease in the size of the urate pool with a concurrent rise in the more soluble xanthine and
hypoxanthine.
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Indications<\/p>\n\n\n\n