Can you take Clobazam with Dezocine?

cloBAZam has a major potential interaction with Acute Alcohol Intoxication.

The use of benzodiazepines with alcohol is not recommended. Patients with acute alcohol intoxication exhibit depressed vital signs. The central nervous system depressant effects of benzodiazepines may be additive with those of alcohol, and severe respiratory depression and death may occur. Therapy with benzodiazepines should be administered cautiously in patients who might be prone to acute alcohol intake.

Dezocine has a major potential interaction with Acute Alcohol Intoxication.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opioid partial agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine has a moderate potential interaction with Adrenal Insufficiency.

Patients with Addison's disease may have increased risk of respiratory depression and prolonged CNS depression associated with the use of narcotic (opioid) analgesic agents. Conversely, these agents may cause or potentiate adrenal insufficiency. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with adrenocortical insufficiency. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

Dezocine has a major potential interaction with Alcoholism.

Opioid partial agonists have the potential to cause dependence and abuse, particularly in patients with a history of drug abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use, and abrupt cessation or a significant reduction in dosage may precipitate withdrawal symptoms. Because of their opioid antagonistic effect, withdrawal symptoms may also occur if opioid partial agonists are administered to patients with an opioid dependence or in whom substantial amounts of narcotics have recently been administered. Therapy with opioid partial agonists is not recommended in patients who are physically dependent on narcotics. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with opioid partial agonists. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of opioid therapy should be undertaken gradually using a dosage-tapering schedule.

Dezocine has a major potential interaction with Altered Consciousness.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opioid partial agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine has a major potential interaction with Asphyxia.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opioid partial agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine has a moderate potential interaction with Biliary Obstruction.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

Dezocine has a major potential interaction with Brain Tumor.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opioid partial agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine has a major potential interaction with Brain Tumor.

The hypoventilation associated with administration of opioid partial agonists can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Unless mechanical ventilation is provided, extreme caution is advised when opioid partial agonists are given to patients with head injury, intracranial lesions, or a preexisting elevated CSF pressure. Also, clinicians treating such patients should be aware that opioid partial agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

Dezocine has a major potential interaction with Cerebral Vascular Disorder.

The hypoventilation associated with administration of opioid partial agonists can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Unless mechanical ventilation is provided, extreme caution is advised when opioid partial agonists are given to patients with head injury, intracranial lesions, or a preexisting elevated CSF pressure. Also, clinicians treating such patients should be aware that opioid partial agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

Dezocine has a major potential interaction with Cerebral Vascular Disorder.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opioid partial agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine has a major potential interaction with Constipation.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

cloBAZam has a moderate potential interaction with Depression.

Benzodiazepines depress the central nervous system and may cause or exacerbate mental depression and cause suicidal behavior and ideation. Episodes of mania and hypomania have also been reported in depressed patients treated with some of these agents. Therapy with benzodiazepines 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.

cloBAZam has a major potential interaction with Drug Dependence.

Benzodiazepines have the potential to cause dependence and abuse. Tolerance as well as physical and psychological dependence can develop, particularly after prolonged use and/or excessive dosages. However, abrupt cessation following continual use of as few as 6 weeks at therapeutic levels has occasionally precipitated withdrawal symptoms. Addiction- prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance when treated with benzodiazepines. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of benzodiazepine therapy should be undertaken gradually using a dosage- tapering schedule. If withdrawal symptoms occur, temporary reinstitution of benzodiazepines may be necessary.

Dezocine has a major potential interaction with Drug Dependence.

Opioid partial agonists have the potential to cause dependence and abuse, particularly in patients with a history of drug abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use, and abrupt cessation or a significant reduction in dosage may precipitate withdrawal symptoms. Because of their opioid antagonistic effect, withdrawal symptoms may also occur if opioid partial agonists are administered to patients with an opioid dependence or in whom substantial amounts of narcotics have recently been administered. Therapy with opioid partial agonists is not recommended in patients who are physically dependent on narcotics. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with opioid partial agonists. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of opioid therapy should be undertaken gradually using a dosage-tapering schedule.

Dezocine has a moderate potential interaction with Gallbladder Disease.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

Dezocine has a major potential interaction with Gastrointestinal Obstruction.

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

Dezocine has a major potential interaction with Gastrointestinal Obstruction.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

Dezocine has a major potential interaction with Head Injury.

The hypoventilation associated with administration of opioid partial agonists can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Unless mechanical ventilation is provided, extreme caution is advised when opioid partial agonists are given to patients with head injury, intracranial lesions, or a preexisting elevated CSF pressure. Also, clinicians treating such patients should be aware that opioid partial agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

Dezocine has a major potential interaction with Head Injury.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opioid partial agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine has a major potential interaction with Infectious Gastroenteritis.

Narcotic (opioid) analgesic agents may prolong and/or worsen diarrhea associated with organisms that invade the intestinal mucosa, such as toxigenic Escherichia coli, Salmonella, Shigella, and pseudomembranous colitis due to broad-spectrum antibiotics. These agents decrease gastrointestinal motility, which may delay the excretion of infective gastroenteric organisms and/or their toxins. Other symptoms and complications such as fever, shedding of organisms, and extraintestinal illness may also be increased or prolonged. Therapy with opioids should be avoided or administered cautiously in patients with infectious diarrhea, particularly that due to pseudomembranous enterocolitis or enterotoxin-producing bacteria or if accompanied by high fever, pus, or blood in the stool.

Dezocine has a major potential interaction with Inflammatory Bowel Disease.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

Dezocine has a major potential interaction with Intestinal Anastomoses.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

Dezocine has a major potential interaction with Ischemic Heart Disease.

Opioid partial agonists may increase systemic and pulmonary arterial pressure and systemic vascular resistance, particularly when given by IV administration. Data are available for pentazocine and butorphanol. Therapy with opioid partial agonists should be administered cautiously and only if the benefit justifies the risk in patients with acute myocardial infarction (especially if accompanied by hypertension or left ventricular failure) or coronary insufficiency.

Dezocine has a moderate potential interaction with Liver Disease.

Narcotic (opioid) analgesic agents are extensively metabolized by the liver, and several of them (e.g., codeine, hydrocodone, meperidine, methadone, morphine, propoxyphene) have active metabolites that are further converted to inactive substances. The serum concentrations of these agents and their metabolites may be increased and the half-lives prolonged in patients with impaired hepatic function. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with liver disease. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

Dezocine has a moderate potential interaction with Pancreatitis.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

Dezocine has a major potential interaction with Prematurity/Underweight in Infancy.

The use of narcotic (opioid) analgesic agents is contraindicated in premature infants. These agents may cross the immature blood-brain barrier to a greater extent than in adults, resulting in disproportionate respiratory depression.

cloBAZam has a moderate potential interaction with Psychosis.

Benzodiazepines depress the central nervous system and may cause or exacerbate mental depression and cause suicidal behavior and ideation. Episodes of mania and hypomania have also been reported in depressed patients treated with some of these agents. Therapy with benzodiazepines 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.

Dezocine has a major potential interaction with Pulmonary Impairment.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opioid partial agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

cloBAZam has a moderate potential interaction with Renal Dysfunction.

Benzodiazepines are excreted by the kidneys and should be used with caution in patients with impaired renal function and end-stage kidney disease.

Dezocine has a moderate potential interaction with Renal Dysfunction.

Although narcotic (opioid) analgesic agents are generally metabolized by the liver, renal impairment can alter the elimination of these agents and their metabolites (some of which are pharmacologically active), resulting in drug accumulation and increased risk of toxicity. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with significantly impaired renal function. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

Dezocine has a major potential interaction with Respiratory Arrest.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opioid partial agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine has a moderate potential interaction with Seizures.

Narcotic (opioid) analgesic agents may increase the frequency of seizures in patients with seizure disorders, may increase the risk of seizures occurring in other clinical settings associated with seizures, and, at higher dosages, have been reported to induce seizures in patients without history of seizures. Patients with history of seizure disorders should be regularly evaluated for worsened seizure control during therapy. Prolonged meperidine use may increase the risk of toxicity (e.g., seizures) from the accumulation of the active metabolite (normeperidine).

Dezocine has a moderate potential interaction with Urinary Retention.

Narcotic (opioid) analgesic agents may inhibit the urinary voiding reflex and increase the tone of the vesical sphincter in the bladder. Acute urinary retention requiring catheterization may occur, particularly in patients with prostatic hypertrophy or urethral stricture and in older adult patients. These agents may also decrease urine production via direct effects on the kidney and central stimulation of the release of vasopressin. Therapy with opioids should be administered cautiously in patients with or predisposed to urinary retention and/or oliguria. The effects on smooth muscle tone appear to be the most pronounced with morphine.