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Abenol (Acetaminophen)
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Pharmacology
Acetaminophen is the major metabolite of phenacetin and acetanilide. Animal and clinical studies have shown acetaminophen to have antipyretic and analgesic activity equal to that of ASA. Acetaminophen lacks anti-inflammatory effects.
Unlike the salicylates, acetaminophen does not interfere with tubular secretion of uric acid nor does it affect acid-base balance if taken in therapeutic doses. Acetaminophen does not interfere with hemostasis and, in particular does not inhibit platelet aggregation. Allergic reactions are rare and thus the drug is useful in patients who cannot tolerate salicylates and those with an allergic diathesis, including bronchial asthmatics. The rate of acetaminophen absorption from the gastrointestinal tract following oral administration is a function of stomach emptying rate and is generally rapid and complete with peak plasma concentrations of free drug being achieved in 0.5 to 1hour following administration. The plasma half-life of unchanged drug is about 2hours, with approximately 85% of a 1g oral dose being recovered in the urine in 24hours. Approximately 3% is excreted unchanged, with the balance being eliminated principally as the glucuronide and sulfate conjugates.
A small portion of the administered acetaminophen is converted by hepatic microsomal enzymes to a reactive metabolite. At therapeutic doses this minor metabolite is rapidly inactivated by conjugation with glutathione and eliminated by renal excretion. However, where hepatic glutathione has been depleted, covalent binding of the reactive metabolite to liver-cell macromolecules occurs and hepatic cell necrosis ensues. It has been shown that glutathione precursors such as N-acetylcysteine, cysteine, cysteamine and methionine can decrease experimental acetaminophen-induced hepatic necrosis when administered promptly after a toxic dose of acetaminophen. Rectal absorption of acetaminophen, as with most rectally administered drugs, is more erratic than absorption following oral administration. Absorption rate is generally slower. Peak blood levels of free acetaminophen are not reached until 1.5to 3hours following rectal administration, and the peak concentration in the blood is approximately 50% of that observed following an equivalent oral dose. The percentage of a rectal dose of acetaminophen absorbed also varies giving wide variances in the bioavailability. In view of these observations, higher rectal doses or more frequent administration may be required to achieve and/or maintain blood concentrations of acetaminophen comparable to those obtained following oral administration.
Acetaminophen is the major metabolite of phenacetin and acetanilide. Animal and clinical studies have shown acetaminophen to have antipyretic and analgesic activity equal to that of ASA. Acetaminophen lacks anti-inflammatory effects.
Unlike the salicylates, acetaminophen does not interfere with tubular secretion of uric acid nor does it affect acid-base balance if taken in therapeutic doses. Acetaminophen does not interfere with hemostasis and, in particular does not inhibit platelet aggregation. Allergic reactions are rare and thus the drug is useful in patients who cannot tolerate salicylates and those with an allergic diathesis, including bronchial asthmatics. The rate of acetaminophen absorption from the gastrointestinal tract following oral administration is a function of stomach emptying rate and is generally rapid and complete with peak plasma concentrations of free drug being achieved in 0.5 to 1hour following administration. The plasma half-life of unchanged drug is about 2hours, with approximately 85% of a 1g oral dose being recovered in the urine in 24hours. Approximately 3% is excreted unchanged, with the balance being eliminated principally as the glucuronide and sulfate conjugates.
A small portion of the administered acetaminophen is converted by hepatic microsomal enzymes to a reactive metabolite. At therapeutic doses this minor metabolite is rapidly inactivated by conjugation with glutathione and eliminated by renal excretion. However, where hepatic glutathione has been depleted, covalent binding of the reactive metabolite to liver-cell macromolecules occurs and hepatic cell necrosis ensues. It has been shown that glutathione precursors such as N-acetylcysteine, cysteine, cysteamine and methionine can decrease experimental acetaminophen-induced hepatic necrosis when administered promptly after a toxic dose of acetaminophen. Rectal absorption of acetaminophen, as with most rectally administered drugs, is more erratic than absorption following oral administration. Absorption rate is generally slower. Peak blood levels of free acetaminophen are not reached until 1.5to 3hours following rectal administration, and the peak concentration in the blood is approximately 50% of that observed following an equivalent oral dose. The percentage of a rectal dose of acetaminophen absorbed also varies giving wide variances in the bioavailability. In view of these observations, higher rectal doses or more frequent administration may be required to achieve and/or maintain blood concentrations of acetaminophen comparable to those obtained following oral administration.
Indications
Acetaminophen Is The Major Metabolite Of Phenacetin And Acetanilide. Animal And Clinical Studies Have Shown Acetaminophen To Have Antipyretic And Analgesic Activity Equal To That Of ASA. Acetaminophen Lacks Anti-inflammatory Effects.
Unlike The Salicylates, Acetaminophen Does Not Interfere With Tubular Secretion Of Uric Acid Nor Does It Affect Acid-base Balance If Taken In Therapeutic Doses. Acetaminophen Does Not Interfere With Hemostasis And, In Particular Does Not Inhibit Platelet Aggregation. Allergic Reactions Are Rare And Thus The Drug Is Useful In Patients Who Cannot Tolerate Salicylates And Those With An Allergic Diathesis, Including Bronchial Asthmatics. The Rate Of Acetaminophen Absorption From The Gastrointestinal Tract Following Oral Administration Is A Function Of Stomach Emptying Rate And Is Generally Rapid And Complete With Peak Plasma Concentrations Of Free Drug Being Achieved In 0.5 To 1hour Following Administration. The Plasma Half-life Of Unchanged Drug Is About 2hours, With Approximately 85% Of A 1g Oral Dose Being Recovered In The Urine In 24hours. Approximately 3% Is Excreted Unchanged, With The Balance Being Eliminated Principally As The Glucuronide And Sulfate Conjugates.
A Small Portion Of The Administered Acetaminophen Is Converted By Hepatic Microsomal Enzymes To A Reactive Metabolite. At Therapeutic Doses This Minor Metabolite Is Rapidly Inactivated By Conjugation With Glutathione And Eliminated By Renal Excretion. However, Where Hepatic Glutathione Has Been Depleted, Covalent Binding Of The Reactive Metabolite To Liver-cell Macromolecules Occurs And Hepatic Cell Necrosis Ensues. It Has Been Shown That Glutathione Precursors Such As N-acetylcysteine, Cysteine, Cysteamine And Methionine Can Decrease Experimental Acetaminophen-induced Hepatic Necrosis When Administered Promptly After A Toxic Dose Of Acetaminophen. Rectal Absorption Of Acetaminophen, As With Most Rectally Administered Drugs, Is More Erratic Than Absorption Following Oral Administration. Absorption Rate Is Generally Slower. Peak Blood Levels Of Free Acetaminophen Are Not Reached Until 1.5to 3hours Following Rectal Administration, And The Peak Concentration In The Blood Is Approximately 50% Of That Observed Following An Equivalent Oral Dose. The Percentage Of A Rectal Dose Of Acetaminophen Absorbed Also Varies Giving Wide Variances In The Bioavailability. In View Of These Observations, Higher Rectal Doses Or More Frequent Administration May Be Required To Achieve And/or Maintain Blood Concentrations Of Acetaminophen Comparable To Those Obtained Following Oral Administration.
Acetaminophen Is The Major Metabolite Of Phenacetin And Acetanilide. Animal And Clinical Studies Have Shown Acetaminophen To Have Antipyretic And Analgesic Activity Equal To That Of ASA. Acetaminophen Lacks Anti-inflammatory Effects.
Unlike The Salicylates, Acetaminophen Does Not Interfere With Tubular Secretion Of Uric Acid Nor Does It Affect Acid-base Balance If Taken In Therapeutic Doses. Acetaminophen Does Not Interfere With Hemostasis And, In Particular Does Not Inhibit Platelet Aggregation. Allergic Reactions Are Rare And Thus The Drug Is Useful In Patients Who Cannot Tolerate Salicylates And Those With An Allergic Diathesis, Including Bronchial Asthmatics. The Rate Of Acetaminophen Absorption From The Gastrointestinal Tract Following Oral Administration Is A Function Of Stomach Emptying Rate And Is Generally Rapid And Complete With Peak Plasma Concentrations Of Free Drug Being Achieved In 0.5 To 1hour Following Administration. The Plasma Half-life Of Unchanged Drug Is About 2hours, With Approximately 85% Of A 1g Oral Dose Being Recovered In The Urine In 24hours. Approximately 3% Is Excreted Unchanged, With The Balance Being Eliminated Principally As The Glucuronide And Sulfate Conjugates.
A Small Portion Of The Administered Acetaminophen Is Converted By Hepatic Microsomal Enzymes To A Reactive Metabolite. At Therapeutic Doses This Minor Metabolite Is Rapidly Inactivated By Conjugation With Glutathione And Eliminated By Renal Excretion. However, Where Hepatic Glutathione Has Been Depleted, Covalent Binding Of The Reactive Metabolite To Liver-cell Macromolecules Occurs And Hepatic Cell Necrosis Ensues. It Has Been Shown That Glutathione Precursors Such As N-acetylcysteine, Cysteine, Cysteamine And Methionine Can Decrease Experimental Acetaminophen-induced Hepatic Necrosis When Administered Promptly After A Toxic Dose Of Acetaminophen. Rectal Absorption Of Acetaminophen, As With Most Rectally Administered Drugs, Is More Erratic Than Absorption Following Oral Administration. Absorption Rate Is Generally Slower. Peak Blood Levels Of Free Acetaminophen Are Not Reached Until 1.5to 3hours Following Rectal Administration, And The Peak Concentration In The Blood Is Approximately 50% Of That Observed Following An Equivalent Oral Dose. The Percentage Of A Rectal Dose Of Acetaminophen Absorbed Also Varies Giving Wide Variances In The Bioavailability. In View Of These Observations, Higher Rectal Doses Or More Frequent Administration May Be Required To Achieve And/or Maintain Blood Concentrations Of Acetaminophen Comparable To Those Obtained Following Oral Administration.
Contraindications
Hypersensitivity to acetaminophen or to its nonmedicinal ingredients.
Hypersensitivity to acetaminophen or to its nonmedicinal ingredients.
Safety Information / Warning
Acetaminophen poisoning can result in severe hepatic damage.
Acetaminophen poisoning can result in severe hepatic damage.
Precautions
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Side Effects / Adverse Effects
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Overdose
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Recommended Dosage
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Supplied / Packaging
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