The plasma half-life is about 2. The remainder of the dose is excreted in the feces. At therapeutic doses, the analgesic effect reaches a peak within 2 hours and persists between 4 and 6 hours. Acetaminophen Acetaminophen is rapidly absorbed from the gastrointestinal tract and is distributed throughout most body tissues. The plasma half-life is 1.

Elimination of acetaminophen is principally by liver metabolism conjugation and subsequent renal excretion of metabolites. Such tasks should be avoided while taking this product. Alcohol and other CNS depressants may produce an additive CNS depression , when taken with this combination product, and should be avoided. Codeine may be habit forming. Patients should take the drug only for as long as it is prescribed, in the amounts prescribed, and no more frequently than prescribed. Caution patients that some people have a variation in a liver enzyme and change codeine into morphine more rapidly and completely than other people.

These people are ultra-rapid metabolizers and are more likely to have higher-than-normal levels of morphine in their blood after taking codeine, which can result in overdose symptoms such as extreme sleepiness, confusion, or shallow breathing.

In most cases, it is unknown if someone is an ultra-rapid codeine metabolizer. Nursing mothers taking codeine can also have higher morphine levels in their breast milk if they are ultra-rapid metabolizers.

These higher levels of morphine in breast milk may lead to life-threatening or fatal side effects in nursing babies. Opiate agonists impair the peristaltic activity of the intestine. Thus, these drugs can antagonize the beneficial actions of bethanechol on GI motility.

Bismuth Subcitrate Potassium; Metronidazole; Tetracycline: Additive constipation may be seen with concurrent use of opiate agonists and antidiarrheals. Bismuth Subsalicylate; Metronidazole; Tetracycline: Close clinical monitoring is advised when administering acetaminophen with boceprevir due to an increased potential for acetaminophen-related adverse events. If acetaminophen dose adjustments are made, re-adjust the dose upon completion of boceprevir treatment.

Although this interaction has not been studied, predictions about the interaction can be made based on the metabolic pathway of acetaminophen. Acetaminophen is partially metabolized by the hepatic isoenzyme CYP3A4; boceprevir inhibits this isoenzyme. Coadministration may result in elevated acetaminophen plasma concentrations.

Due to the CNS effects of brexpiprazole, caution is advisable when brexpiprazole is given in combination with other centrally-acting medications including opiate agonists.

Based on the sedative effects of brimonidine in individual patients, brimonidine administration has potential to enhance the CNS depressants effects of opiate agonists. Drowsiness has been reported during administration of carbetapentane. An enhanced CNS depressant effect may occur when carbetapentane is combined with other CNS depressants including morphine. In some cases of acute pain, trauma, or during surgical management, opiate-dependent patients receiving buprenorphine maintenance therapy may require concurrent treatment with opiate agonists, such as codeine.

In these cases, health care professionals must exercise caution in opiate agonist dose selection, as higher doses of an opiate agonist may be required to compete with buprenorphine at the mu-receptor. Management strategies may include adding a short-acting opiate agonist to achieve analgesia in the presence of buprenorphine, discontinuation of buprenorphine and use of an opiate agonist to avoid withdrawal and achieve analgesia, or conversion of buprenorphine to methadone while using additional opiate agonists if needed.

Closely monitor patients for CNS or respiratory depression. When buprenorphine is used for analgesia, avoid co-use with opiate agonists.

Buprenorphine may cause withdrawal symptoms in patients receiving chronic opiate agonists as well as possibly potentiate CNS, respiratory, and hypotensive effects. Naloxone can antagonize the therapeutic efficacy of codeine in addition to precipitating withdrawal symptoms in patients who are physically dependent on opiate drugs including codeine. Patients receiving inhibitors of the CYP2D6 isoenzyme, like bupropion, will have a reduction in the metabolic conversion of codeine to morphine and therefore may not experience an adequate analgesic response to codeine.

When naltrexone is used as adjuvant treatment of opiate or alcohol dependence, use is contraindicated in patients currently receiving opiate agonists. Naltrexone will antagonize the therapeutic benefits of opiate agonists and will induce a withdrawal reaction in patients with physical dependence to opioids. An opiate antagonist should only be administered to a patient taking codeine with clinically significant respiratory or cardiovascular depression.

Also, patients should be opiate-free for at least days prior to initiating naltrexone therapy. If a patient receives naltrexone, and an opiate agonist is needed for an emergency situation, large doses of opiate agonists may ultimately overwhelm naltrexone antagonism of opiate receptors. Immediately following administration of exogenous opiate agonists, the opiate plasma concentration may be sufficient to overcome naltrexone competitive blockade, but the patient may experience deeper and more prolonged respiratory depression and thus, may be in danger of respiratory arrest and circulatory collapse.

Non-receptor mediated actions like facial swelling, itching, generalized erythema, or bronchoconstriction may occur presumably due to histamine release. A rapidly acting opiate agonist is preferred as the duration of respiratory depression will be shorter. Patients receiving naltrexone may also experience opiate side effects with low doses of opiate agonists.

If the opiate agonist is taken in such a way that high concentrations remain in the body beyond the time naltrexone exerts its therapeutic effects, serious side effects may occur.

Concomitant use of CNS depressants, such as buspirone, can potentiate the effects of codeine, which may potentially lead to respiratory depression, CNS depression, sedation, or hypotensive responses.

If concurrent use of codeine and buspirone is imperative, reduce the dose of one or both drugs. Use busulfan and acetaminophen together with caution; concomitant use may result in increased busulfan levels and increased busulfan toxicity. Separating the administration of these drugs may mitigate this interaction; avoid giving acetaminophen within 72 hours prior to or concurrently with busulfan.

Busulfan is metabolized in the liver through conjugation with glutathione; acetaminophen decreases glutathione levels in the blood and tissues and may reduce the clearance of busulfan. Avoid the concomitant use of butorphanol and opiate agonists, such as codeine. Butorphanol may cause withdrawal symptoms in patients receiving chronic opiate agonists. Concurrent use of butorphanol with other opiate agonists can cause additive CNS, respiratory, and hypotensive effects.

Inducers of CYP3A4 such as carbamazepine, may induce the hepatic metabolism of opiate agonists, which may lead to opiate withdrawal or inadequate pain control. This interaction is most significant if the enzyme-inducing agent is added after opiate therapy has begun in patients who are opiate tolerant. Clinicians should be alert to changes in the effect of the opioid agonist.

Opiate doses may need to be increased if carbamazepine is added. Conversely, doses may need to be decreased if carbamazepine is discontinued. Carbamazepine may potentially accelerate the hepatic metabolism of acetaminophen.

In addition, due to enzyme induction, carbamazepine may increase the risk for acetaminophen-induced hepatotoxicity via generation of a greater percentage of acetaminophen's hepatotoxic metabolite, NAPQI.

Clinicians should be alert to decreased effect of acetaminophen. Concomitant use of opiate agonists with other central nervous system CNS depressants such as COMT inhibitors can potentiate the effects of the opiate and may lead to additive CNS or respiratory depression, profound sedation, or coma. Prior to concurrent use of an opiate in patients taking a CNS depressant, assess the level of tolerance to CNS depression that has developed, the duration of use, and the patient's overall response to treatment.

Carefully monitor the patient for hypotension, CNS depression, and respiratory depression. Carbon dioxide retention from opioid-induced respiratory depression can exacerbate the sedating effects of opioids. Due to the CNS effects of cariprazine, caution is advisable when cariprazine is given in combination with other centrally-acting medications including opiate agonists.

Additive drowsiness may occur if cetirizine or levocetirizine is administered with other drugs that depress the CNS, including opiate agonists. Activated charcoal binds many drugs within the gut.

Administering charcoal dietary supplements at the same time as a routine acetaminophen dosage would be expected to interfere with the analgesic and antipyretic efficacy of acetaminophen. Charcoal is mostly used in the setting of acetaminophen overdose; however, patients should never try to treat an acetaminophen overdose with charcoal dietary supplements.

Advise patients to get immediate medical attention for an acetaminophen overdose. Due to the CNS depression potential of all local anesthetics, they should be used with caution with other agents that can cause respiratory depression, such as opiate agonists. The activity of codeine is due to its conversion to morphine via the cytochrome P 2D6 hepatic isoenzyme. Chloroquine inhibits CYP2D6 and may theoretically decrease the conversion of codeine to morphine.

Chlorpheniramine; Guaifenesin; Hydrocodone; Pseudoephedrine: Phenothiazines can potentiate the CNS depressant action of other drugs such as opiate agonists. Clonidine has CNS depressive effects and can potentiate the actions of other CNS depressants including opiate agonists. Experts have recommended that cholestyramine not be given within 1 hour of acetaminophen if analgesic or antipyretic effect is to be achieved. Choline Salicylate; Magnesium Salicylate: Cimetidine may inhibit the conversion of codeine to morphine, codeine's active metabolite, via the CYP2D6 hepatic isoenzyme and therefore may decrease the ability for codeine to produce analgesic effect.

Cinacalcet, a strong in vitro inhibitor of the CYP2D6 cytochrome P enzyme, may theoretically increase serum concentrations of other drugs metabolized by this enzyme, including codeine. Impairment of CYP2D6 metabolism by citalopram may reduce the conversion of the opiates codeine and hydrocodone to their active forms, thus reducing analgesic efficacy.

Concomitant use of central nervous system depressants, such as clozapine, can potentiate the effects of codeine, which may lead to respiratory depression, CNS depression, sedation, or hypotensive responses. Combining clozapine with opiate agonists may also lead to additive effects on intestinal motility or bladder function, resulting in constipation or urinary retention.

Cobicistat; Elvitegravir; Emtricitabine; Tenofovir Alafenamide: Pharmacodynamic interactions between crofelemer and opiate agonists are theoretically possible. Crofelemer does not affect GI motility mechanisms, but does have antidiarrheal effects. Patients taking medications that decrease GI motility, such as opiate agonists, may be at greater risk for serious complications from crofelemer, such as constipation with chronic use. Use caution and monitor GI symptoms during coadministration.

Dasabuvir; Ombitasvir; Paritaprevir; Ritonavir: Concurrent administration of acetaminophen with ritonavir may result in elevated acetaminophen plasma concentrations and subsequent adverse events. Acetaminophen is metabolized by the hepatic isoenzyme CYP3A4; ritonavir is an inhibitor of this enzyme.

Caution and close monitoring are advised if these drugs are administered together. Delavirdine may decrease the efficacy of codeine-containing analgesics by inhibiting the conversion of codeine to morphine via CYP2D6. Codeine has a low affinity for CYP2D6; therefore, its analgesic activity may vary greatly when it is combined with any other drugs that inhibit CYP2D6, such as delavirdine.

Concurrent use with opiate agonists can decrease the minimum alveolar concentration MAC of desflurane needed to produce anesthesia. Although desloratadine is considered a 'non-sedating' antihistamine, rare CNS effects such as dizziness and sedation have been reported.

For this reason, it would be prudent to monitor for drowsiness or dizziness when used concurrently with other CNS depressants such as opiate agonists. Quick GuideChronic Pain Syndrome: If any of these effects persist or worsen, notify your doctor or pharmacist promptly. Remember that your doctor has prescribed this medication because he or she has judged that the benefit to you is greater than the risk of side effects.

Many people using this medication do not have serious side effects. Tell your doctor immediately if any of these unlikely but serious side effects occur: If you do not have liver problems, the adult maximum dose of acetaminophen is 4 grams milligrams.

If you take more than the maximum daily amount, it may cause serious possibly fatal liver disease. This can be life-threatening. Do not give to a child younger than 12 years of age. Some children have had very bad and sometimes deadly breathing problems when using codeine after surgery to remove tonsils or adenoids.

Do not give to a child younger than 18 years of age who has had surgery to remove tonsils or adenoids. Talk with your child's doctor. It is used to ease pain. If you are allergic to any drugs like this one, any other drugs, foods, or other substances.

Tell your doctor about the allergy and what signs you had, like rash; hives ; itching; shortness of breath; wheezing; cough; swelling of face, lips, tongue, or throat; or any other signs. If you have any of these health problems: Lung or breathing problems like asthma , trouble breathing, or sleep apnea; high levels of carbon dioxide in the blood; or stomach or bowel block or narrowing.

If you are taking any of these drugs: Buprenorphine , butorphanol , nalbuphine , or pentazocine. If you have taken certain drugs used for low mood depression like isocarboxazid , phenelzine , or tranylcypromine or drugs used for Parkinson's disease like selegiline or rasagiline in the last 14 days. Codeine may also cause severe, possibly fatal, breathing problems.

To lower your risk, your doctor should have you take the smallest dose of codeine that works, and take it for the shortest possible time. See also How to Use section for more information about addiction.

Taking this medication with alcohol or other drugs that can cause drowsiness or breathing problems may cause very serious side effects, including death. Also, other medications can affect the removal of codeine from your body, which may affect how codeine works. Acetaminophen and codeine is a combination medicine used to relieve moderate to severe pain. Acetaminophen and codeine may also be used for other purposes not listed in this medication guide.

You should not use this medicine if you have recently used alcohol, sedatives, tranquilizers, or other narcotic medications. This medicine is not for use in children younger than 12 years old, and is not for use in anyone under 18 who recently had surgery to remove the tonsils or adenoids. Taking this medicine during pregnancy may cause life-threatening withdrawal symptoms in the newborn.

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