Drug Interactions between hydroxyzine and tramadol

Do not use alcohol or medications that contain alcohol while you are receiving treatment with traMADol. This may increase nervous system side effects such as drowsiness, dizziness, lightheadedness, difficulty concentrating, and impairment in thinking and judgment. In severe cases, low blood pressure, respiratory distress, fainting, coma, or even death may occur. You should also avoid consuming grapefruit and grapefruit juice, as this may increase the blood levels and effects of traMADol. If you are taking an extended-release formulation, the pill should be swallowed whole (i.E., do not crush, chew, or divide the pill). Talk to your doctor or pharmacist if you have questions on how to take this or other medications you are prescribed. Do not exceed the dose of traMADol prescribed for you or use the medication more frequently or for a longer duration than prescribed by your doctor. Also avoid activities requiring mental alertness such as driving or operating hazardous machinery until you know how the medication affects you. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medication without first talking to your doctor.

Alcohol can increase the nervous system side effects of hydrOXYzine such as dizziness, drowsiness, and difficulty concentrating. Some people may also experience impairment in thinking and judgment. You should avoid or limit the use of alcohol while being treated with hydrOXYzine. Do not use more than the recommended dose of hydrOXYzine, and avoid activities requiring mental alertness such as driving or operating hazardous machinery until you know how the medication affects you. Talk to your doctor or pharmacist if you have any questions or concerns.

Tramadol exposes patients and other users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing tramadol, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed tramadol, but use in such patients requires intensive counseling about the risks and proper use of tramadol, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered.

Opioids are sought by drug abusers and patients with addiction disorders and are subject to criminal diversion. These risks should be considered when prescribing or dispensing tramadol. Strategies to reduce such risks include prescribing the smallest appropriate quantity and advising the patient about proper disposal of unused drug.

The CNS depressant effects of tramadol may be additive with those of alcohol and may lead to profound sedation, respiratory depression, coma, and death. Therapy with tramadol should be administered cautiously (and only when alternative treatment options are inadequate) in patients who might be prone to acute alcohol intake. Dosages and durations should be limited to the minimum required and patients should be monitored for signs and symptoms of respiratory depression and sedation. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; naloxone will reverse some, but not all, symptoms caused by overdosage with tramadol, but it also increases the risk of seizures.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

A variety of abnormal thinking and behavior changes have been reported to occur in association with the use of most anxiolytics, sedatives and hypnotics. Some of these changes include decreased inhibition, aggressiveness, agitation, and hallucinations. These drugs can cause or exacerbate mental depression and cause suicidal behavior and ideation. Therapy with these drugs should be administered cautiously in patients with a history of depression or other psychiatric disorders. Patients should be monitored for any changes in mood or behavior. It may be prudent to refrain from dispensing large quantities of medication to these patients.

Tramadol exposes patients and other users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing tramadol, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed tramadol, but use in such patients requires intensive counseling about the risks and proper use of tramadol, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered.

Opioids are sought by drug abusers and patients with addiction disorders and are subject to criminal diversion. These risks should be considered when prescribing or dispensing tramadol. Strategies to reduce such risks include prescribing the smallest appropriate quantity and advising the patient about proper disposal of unused drug.

Tramadol exposes patients and other users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing tramadol, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed tramadol, but use in such patients requires intensive counseling about the risks and proper use of tramadol, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered.

Opioids are sought by drug abusers and patients with addiction disorders and are subject to criminal diversion. These risks should be considered when prescribing or dispensing tramadol. Strategies to reduce such risks include prescribing the smallest appropriate quantity and advising the patient about proper disposal of unused drug.

Opioid analgesics are contraindicated in patients with known or suspected gastrointestinal obstruction, including paralytic ileus.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

Hydroxyzine is contraindicated in patients with a QT prolonged interval. Cases of QT prolongation and Torsade de Pointes have been reported during postmarketing studies. Most of the cases reported occurred in patients with other risk factors for QT prolongation, such as preexisting heart disease, electrolyte imbalances or arrhythmogenic drug use. Therefore, hydroxyzine should be used with caution in patients with risk factors for QT prolongation, congenital long QT syndrome, family history of long QT syndrome or other predisposing conditions, as well as myocardial infarction, uncompensated heart failure, and bradyarrhythmias.

Tramadol exposes patients and other users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing tramadol, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed tramadol, but use in such patients requires intensive counseling about the risks and proper use of tramadol, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered.

Opioids are sought by drug abusers and patients with addiction disorders and are subject to criminal diversion. These risks should be considered when prescribing or dispensing tramadol. Strategies to reduce such risks include prescribing the smallest appropriate quantity and advising the patient about proper disposal of unused drug.

Hydroxyzine is contraindicated in patients with a QT prolonged interval. Cases of QT prolongation and Torsade de Pointes have been reported during postmarketing studies. Most of the cases reported occurred in patients with other risk factors for QT prolongation, such as preexisting heart disease, electrolyte imbalances or arrhythmogenic drug use. Therefore, hydroxyzine should be used with caution in patients with risk factors for QT prolongation, congenital long QT syndrome, family history of long QT syndrome or other predisposing conditions, as well as myocardial infarction, uncompensated heart failure, and bradyarrhythmias.

Hydroxyzine is contraindicated in patients with a QT prolonged interval. Cases of QT prolongation and Torsade de Pointes have been reported during postmarketing studies. Most of the cases reported occurred in patients with other risk factors for QT prolongation, such as preexisting heart disease, electrolyte imbalances or arrhythmogenic drug use. Therefore, hydroxyzine should be used with caution in patients with risk factors for QT prolongation, congenital long QT syndrome, family history of long QT syndrome or other predisposing conditions, as well as myocardial infarction, uncompensated heart failure, and bradyarrhythmias.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

Tramadol is contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with tramadol. Patients should be monitored closely for respiratory depression, especially within the first 24 to 72 hours of initiating therapy and after a dosage increase.

The use of tramadol in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Tramadol-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of tramadol. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), tramadol may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting tramadol.

Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating tramadol and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered.

Hydroxyzine is contraindicated in patients with a QT prolonged interval. Cases of QT prolongation and Torsade de Pointes have been reported during postmarketing studies. Most of the cases reported occurred in patients with other risk factors for QT prolongation, such as preexisting heart disease, electrolyte imbalances or arrhythmogenic drug use. Therefore, hydroxyzine should be used with caution in patients with risk factors for QT prolongation, congenital long QT syndrome, family history of long QT syndrome or other predisposing conditions, as well as myocardial infarction, uncompensated heart failure, and bradyarrhythmias.

Seizures have been reported in patients receiving tramadol within the recommended dosage range. The risk appears to increase with doses above the recommended range and with concomitant use of certain drugs (e.g., those that reduce the seizure threshold). Risk of seizure may also increase in patients with epilepsy, those with a history of seizures, or in patients with a recognized risk for seizure (e.g., head trauma, metabolic disorders, alcohol and drug withdrawal, CNS infections). In tramadol overdose, naloxone administration may increase the risk of seizures.

Tramadol should not be prescribed for patients who are suicidal or addiction-prone. The use of nonnarcotic analgesics should be considered for patients who are suicidal or depressed. Tramadol should be prescribed with caution for patients with history of misuse and/or are currently taking CNS-active drugs, antidepressant drugs, alcohol in excess, and patients who suffer from emotional disturbance or depression. Patients should be advised not to exceed the recommended dose and to limit their intake of alcohol.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

Tramadol may cause spasm of the sphincter of Oddi. Opioids may increase serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be monitored for worsening symptoms.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

Seizures have been reported in patients receiving tramadol within the recommended dosage range. The risk appears to increase with doses above the recommended range and with concomitant use of certain drugs (e.g., those that reduce the seizure threshold). Risk of seizure may also increase in patients with epilepsy, those with a history of seizures, or in patients with a recognized risk for seizure (e.g., head trauma, metabolic disorders, alcohol and drug withdrawal, CNS infections). In tramadol overdose, naloxone administration may increase the risk of seizures.

Tramadol may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating tramadol. In patients with circulatory shock, tramadol may cause vasodilation that can further reduce cardiac output and blood pressure; tramadol should be avoided in patients with circulatory shock.

Tramadol should not be prescribed for patients who are suicidal or addiction-prone. The use of nonnarcotic analgesics should be considered for patients who are suicidal or depressed. Tramadol should be prescribed with caution for patients with history of misuse and/or are currently taking CNS-active drugs, antidepressant drugs, alcohol in excess, and patients who suffer from emotional disturbance or depression. Patients should be advised not to exceed the recommended dose and to limit their intake of alcohol.

Cases of tramadol-associated hypoglycemia have been reported, some resulting in hospitalization. In most cases, patients had predisposing risk factors (e.g., diabetes); caution is recommended in these patients. If hypoglycemia is suspected, blood glucose levels should be monitored and discontinuation of therapy should be considered as appropriate.

Seizures have been reported in patients receiving tramadol within the recommended dosage range. The risk appears to increase with doses above the recommended range and with concomitant use of certain drugs (e.g., those that reduce the seizure threshold). Risk of seizure may also increase in patients with epilepsy, those with a history of seizures, or in patients with a recognized risk for seizure (e.g., head trauma, metabolic disorders, alcohol and drug withdrawal, CNS infections). In tramadol overdose, naloxone administration may increase the risk of seizures.

Tramadol may cause spasm of the sphincter of Oddi. Opioids may increase serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be monitored for worsening symptoms.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

Some hypnotic drugs can have an anticholinergic effect and should be used with caution in patients with glaucoma, and trouble urinating due to retention or enlarged prostate.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

Opioids may obscure the clinical course in a patient with a head injury. The use of tramadol should be avoided in patients with impaired consciousness or coma.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

Tramadol may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating tramadol. In patients with circulatory shock, tramadol may cause vasodilation that can further reduce cardiac output and blood pressure; tramadol should be avoided in patients with circulatory shock.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

Opioids may obscure the clinical course in a patient with a head injury. The use of tramadol should be avoided in patients with impaired consciousness or coma.

Tramadol is converted by the liver to several metabolites, one of which (referred to as M1) is pharmacologically active and a more potent analgesic than tramadol itself. The metabolism of both tramadol and M1 has been shown to decrease in patients with advanced cirrhosis of the liver, resulting in increased exposure to tramadol as well as substantially prolonged elimination half-lives for both tramadol and M1. Therapy with tramadol should be administered cautiously in patients with liver dysfunction. In patients with severe liver dysfunction, dosage reduction is recommended with the immediate-release formulations, while the extended-release formulations should not be used.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

Some anxiolytics, sedatives and hypnotics are extensively metabolized by the liver, and excreted in the urine. Patients with impaired renal and/or hepatic function may be at greater risk for adverse effects, including central nervous system and respiratory depression, due to drug and metabolite accumulation. Therapy with these drugs should be administered cautiously in such patients, with careful dose selection usually starting at the low end of the dosing range.

In general, anxiolytics, sedatives and hypnotics are extensively metabolized by the liver. Their plasma clearance may be decreased and their half-life prolonged in patients with impaired hepatic function. Therapy with these drugs should be administered cautiously in patients with liver disease (some are not recommended in severe liver impairment), and the dosage should be adjusted accordingly. Laboratory testing is recommended prior and during treatment.

Tramadol may cause spasm of the sphincter of Oddi. Opioids may increase serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be monitored for worsening symptoms.

Tramadol should not be prescribed for patients who are suicidal or addiction-prone. The use of nonnarcotic analgesics should be considered for patients who are suicidal or depressed. Tramadol should be prescribed with caution for patients with history of misuse and/or are currently taking CNS-active drugs, antidepressant drugs, alcohol in excess, and patients who suffer from emotional disturbance or depression. Patients should be advised not to exceed the recommended dose and to limit their intake of alcohol.

Some anxiolytics, sedatives and hypnotics are extensively metabolized by the liver, and excreted in the urine. Patients with impaired renal and/or hepatic function may be at greater risk for adverse effects, including central nervous system and respiratory depression, due to drug and metabolite accumulation. Therapy with these drugs should be administered cautiously in such patients, with careful dose selection usually starting at the low end of the dosing range.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

Tramadol and its metabolites, one of which (referred to as M1) is pharmacologically active and a more potent analgesic than tramadol itself, are primarily excreted in the urine. The rate and extent of excretion of both tramadol and M1 have been shown to decrease in patients with impaired renal function. Therapy with tramadol should be administered cautiously in such patients. In patients with CrCl less than 30 mL/min, dosage reduction is recommended with the immediate-release formulations, while the extended-release formulations should not be used.

Tramadol may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating tramadol. In patients with circulatory shock, tramadol may cause vasodilation that can further reduce cardiac output and blood pressure; tramadol should be avoided in patients with circulatory shock.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

Some hypnotic drugs can have an anticholinergic effect and should be used with caution in patients with glaucoma, and trouble urinating due to retention or enlarged prostate.