Acetaminophen Aspirin Codeine
Name: Acetaminophen Aspirin Codeine
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- Acetaminophen Aspirin Codeine 50 mg
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Acetaminophen Aspirin Codeine Description
Acetaminophen, aspirin, and codeine phosphate capsules are available in three different strengths and colors:
150 mg/180 mg/15 mg 150 mg/180 mg/30 mg 150 mg/180 mg/60 mg
(grey/green) (grey/black) (grey/red)
Acetaminophen 150 mg 150 mg 150 mg
Aspirin 180 mg 180 mg 180 mg
Codeine* Phosphate 15 mg 30 mg 60 mg
(*WARNING: May be habit forming)
Also contains pregelatinized starch and sodium lauryl sulfate with capsule shells composed of gelatin (containing silicon dioxide and sodium lauryl sulfate as manufacturing aides to the gelatin) with black iron oxide and titanium dioxide as color additives. In addition, the capsule containing 15 mg of codeine phosphate also contains: D&C Yellow #10, FD&C Blue #1 and FD&C Red #40. The capsule containing 60 mg codeine phosphate also contains: FD&C Blue #1 and FD&C Red #40.
Acetaminophen, 4′-hydroxyacetanilide, is a non-opiate, non-salicylate analgesic and antipyretic which occurs as a white, odorless, crystalline powder, possessing a slightly bitter taste. Its structure is as follows:
C8H9NO2 M.W. 151.16
Aspirin, salicylic acid acetate, is a non-opiate analgesic, anti-inflammatory and antipyretic agent. It occurs as a white, crystalline tabular or needle-like powder and is odorless or has a faint odor, Its structure is as follows:
C9H8O4 MW. 180.16
Codeine is an alkaloid, obtained from opium or prepared from morphine by methylation. Codeine phosphate occurs as fine, white, needle-shaped crystals, or white, crystalline powder. It is affected by light. Its chemical name is: 7,8-didehydro-4,5α-epoxy-3-methoxy-17-methylmorphinan-6α-ol phosphate (1:1) (salt) hemihydrate. Its structure is as follows:
C18H21NO3•H3PO4•1/2 H2O M.W. 406.37
Acetaminophen Aspirin Codeine - Clinical Pharmacology
Acetaminophen, aspirin, and codeine phosphate capsules combine the analgesic effects of a centrally acting analgesic, codeine, with the peripherally acting analgesics, acetaminophen and aspirin. All ingredients are well absorbed orally. The plasma elimination half-life ranges from 1 to 4 hours for acetaminophen, and from 2.5 to 3 hours for codeine. Although aspirin has a half-life of only about 15 minutes, the apparent biologic half-life of salicylic acid in the therapeutic plasma concentration range is between 6 and 12 hours.
Codeine retains at least one-half of its analgesic activity when administered orally. A reduced first-pass metabolism of codeine by the liver accounts for the greater oral efficacy of codeine when compared to most other morphine-like narcotics. Following absorption, codeine is metabolized by the liver and metabolic products are excreted in the urine. Approximately 10 percent of the administered codeine is demethylated to morphine, which may account for its analgesic activity.
Acetaminophen is distributed throughout most fluids of the body, and is metabolized primarily in the liver. Little unchanged drug is excreted in the urine, but most metabolic products appear in the urine within 24 hours.
Aspirin is rapidly absorbed and almost totally hydrolyzed to salicylic acid following oral administration. Salicylic acid is eliminated by renal excretion and by biotransformation to inactive metabolites. Clearance of salicylic acid in the high-dose range is sensitive to urinary pH and is reduced by renal dysfunction.
Drug Abuse and Dependence
Acetaminophen, aspirin, and codeine phosphate capsules are a Schedule III controlled substance.
Codeine can produce drug dependence of the morphine type, and therefore has the potential for being abused. Psychic dependence, physical dependence and tolerance may develop upon repeated administration of this drug, and it should be prescribed and administered with the same degree of caution appropriate to the use of other oral narcotic-containing medications.
Signs and Symptoms: In acute acetaminophen overdosage, dose-dependent, potentially fatal hepatic necrosis is the most serious adverse effect. Renal tubular necrosis, hypoglycemic coma and thrombocytopenia may also occur.
In adults, hepatic toxicity has rarely been reported with acute overdoses of less than 10 grams and fatalities with less than 15 grams. Importantly, young children seem to be more resistant than adults to the hepatotoxic effect of an acetaminophen overdose. Despite this, the measures outlined below should be initiated in any adult or child suspected of having ingested an acetaminophen overdose.
Early symptoms following a potentially hepatotoxic overdose may include: nausea, vomiting, diaphoresis and general malaise. Clinical and laboratory evidence of hepatic toxicity may not be apparent until 48 to 72 hours post-ingestion.
Treatment: The stomach should be emptied promptly by lavage or by induction of emesis with syrup of ipecac. Patients’ estimates of the quantity of drug ingested are notoriously unreliable. Therefore, if an acetaminophen overdose is suspected, a serum acetaminophen assay should be obtained as early as possible, but no sooner than four hours following ingestion. Liver function studies should be obtained initially and repeated at 24-hour intervals.
The antidote, N-acetylcysteine, should be administered as early as possible, preferably within 16 hours of the overdose ingestion for optimal results, but in any case, within 24 hours. Following recovery, there are no residual, structural or functional hepatic abnormalities.
Signs and Symptoms: Headache, tinnitus, hearing difficulty, dim vision, dizziness, lassitude, hyperpnea, rapid breathing, thirst, nausea, vomiting, sweating and occasionally diarrhea are characteristic of mild to moderate salicylate poisoning. Salicylate poisoning should be considered in children with symptoms of vomiting, hyperpnea, and hyperthermia.
Hyperpnea is an early sign of salicylate poisoning, but dyspnea supervenes at plasma levels above 50 mg/dL. These respiratory changes eventually lead to serious acid-base disturbances. Metabolic acidosis is a constant finding in infants but occurs in older children only with severe poisoning; adults usually exhibit respiratory alkalosis initially and acidosis terminally.
Other symptoms of severe salicylate poisoning include hyperthermia, dehydration, delirium, and mental disturbances. Skin eruptions, GI hemorrhage, or pulmonary edema are less common. Early CNS stimulation is replaced by increasing depression, stupor, and coma. Death is usually due to respiratory failure or cardiovascular collapse.
Treatment: Since there are no specific antidotes for salicylate poisoning, the aim of treatment is to enhance elimination of salicylate and prevent or reduce further absorption; to correct any fluid electrolyte or metabolic imbalance; and to provide general and cardiorespiratory support. If acidosis is present, intravenous sodium bicarbonate must be given, along with adequate hydration, until salicylate levels decrease to within the therapeutic range. To enhance elimination, forced diuresis and alkalinization of the urine may be beneficial. The need for hemoperfusion or hemodialysis is rare and should be used only when other measures have tailed.
Signs andSymptoms: Serious overdose with codeine is characterized by respiratory depression (a decrease in respiratory rate and/or tidal volume, Cheyne-Stokes respiration, cyanosis), extreme somnolence progressing to stupor or coma, skeletal muscle flaccidity, cold and clammy skin, and sometimes bradycardia and hypotension. In severe overdosage, apnea, circulatory collapse, cardiac arrest and death may occur.
Treatment: Primary attention should be given to the reestablishment of adequate respiratory exchange through provision of a patent airway and the institution of assisted or controlled ventilation. The narcotic antagonist naloxone is a specific antidote against respiratory depression which may result from overdosage or unusual sensitivity to narcotics, including codeine. Therefore, an appropriate dose of naloxone hydrochloride (see package insert) should be administered, preferably by the intravenous route, and simultaneously with efforts at respiratory resuscitation. Since the duration of action of codeine may exceed that of the antagonist, the patient should be kept under continued surveillance and repeated doses of the antagonist should be administered as needed to maintain adequate respiration.
An antagonist should not be administered in the absence of clinically significant respiratory or cardiovascular depression. Oxygen, intravenous fluids, vasopressors and other supportive measures should be employed as indicated.
Gastric emptying may be useful in removing unabsorbed drug.
Acetaminophen Aspirin Codeine Dosage and Administration
Dosage should be adjusted according to severity of pain and response of the patient. It should be kept in mind, however, that tolerance to codeine can develop with continued use and that the incidence of untoward effects is dose related. Adult doses of codeine higher than 60 mg fail to give commensurate relief of pain but merely prolong analgesia and are associated with an appreciably increased incidence of undesirable side effects. Equivalently high doses in children would have similar effects.
The dose of this combination product is limited by the amount of codeine phosphate per capsule. For adults, a single dose of codeine phosphate should not exceed 60 mg. For children, the usual recommended single dose is 0.5 mg/kg.
For the capsule containing 15 mg or 30 mg of codeine phosphate, the usual adult dosage is one or two capsules every four hours as needed.
For the capsule containing 60 mg of codeine phosphate, the usual adult dosage is one capsule every four hours as needed.