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79 Cards in this Set
- Front
- Back
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63. BZDs?
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a. Commonly used in tx of anxiety disorders.
b. Easily obtained via prescription from physician offices and emergency departments. |
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64. MOA of BZDs?
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a. Potentiate the effects of GABA by ↑ the frequency of chloride channel opening.
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65. Use of Barbiturates?
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a. Used in the tx of epilepsy and as anaesthetics.
b. Potentiate the effects of GABA by ↑ the duration of chloride channel opening. c. At high doses, barbiturates act as direct GABA agonists and have a lower margin of safety relative to BZDs. |
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66. Synergism of barbiturates?
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a. They are synergistic in combination w/BZDs and barbiturates (as well as other CNS depressants).
b. Respiratory depression can occur as a complication. |
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67. Intoxication w/sedative hypnotics?
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a. Drowsiness/confusion.
b. Hypotension c. Slurred speech d. Incoordination e. Ataxia f. Mood lability g. Impaired judgement h. Nystagmus i. Respiratory depression j. Coma or death in overdose. |
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63. BZDs?
|
a. Commonly used in tx of anxiety disorders.
b. Easily obtained via prescription from physician offices and emergency departments. |
|
|
68. Tx of sedative-hypnotic intoxication?
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a. Maintain airway, breathing, and circulation. Monitor vital signs.
b. Activated charcoal and gastric lavage to prevent further GI absorption (if drug was ingested in the prior 4-6 hrs). |
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64. MOA of BZDs?
|
a. Potentiate the effects of GABA by ↑ the frequency of chloride channel opening.
|
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65. Use of Barbiturates?
|
a. Used in the tx of epilepsy and as anaesthetics.
b. Potentiate the effects of GABA by ↑ the duration of chloride channel opening. c. At high doses, barbiturates act as direct GABA agonists and have a lower margin of safety relative to BZDs. |
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69. Tx for barbiturates ONLY?
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a. Alkalinize urine w/sodium bicarbonate to promote renal excretion.
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66. Synergism of barbiturates?
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a. They are synergistic in combination w/BZDs and barbiturates (as well as other CNS depressants).
b. Respiratory depression can occur as a complication. |
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70. Tx for BZDs only?
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a. Flumazenil in overdose.
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67. Intoxication w/sedative hypnotics?
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a. Drowsiness/confusion.
b. Hypotension c. Slurred speech d. Incoordination e. Ataxia f. Mood lability g. Impaired judgement h. Nystagmus i. Respiratory depression j. Coma or death in overdose. |
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71. Sedative-hypnotic withdrawal?
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a. Abrupt abstinence after chronic use can be life threatening.
b. While physiological dependence is more likely w/short-acting agents, longer-acting agents can also cause dependence and withdrawal sx. |
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68. Tx of sedative-hypnotic intoxication?
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a. Maintain airway, breathing, and circulation. Monitor vital signs.
b. Activated charcoal and gastric lavage to prevent further GI absorption (if drug was ingested in the prior 4-6 hrs). |
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72. GHB?
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a. GHB is a dose-specific CNS depressant that produces memory loss, respiratory distress, and coma.
b. It is commonly used as a date-rape drug. |
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69. Tx for barbiturates ONLY?
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a. Alkalinize urine w/sodium bicarbonate to promote renal excretion.
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70. Tx for BZDs only?
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a. Flumazenil in overdose.
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71. Sedative-hypnotic withdrawal?
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a. Abrupt abstinence after chronic use can be life threatening.
b. While physiological dependence is more likely w/short-acting agents, longer-acting agents can also cause dependence and withdrawal sx. |
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72. GHB?
|
a. GHB is a dose-specific CNS depressant that produces memory loss, respiratory distress, and coma.
b. It is commonly used as a date-rape drug. |
|
|
63. BZDs?
|
a. Commonly used in tx of anxiety disorders.
b. Easily obtained via prescription from physician offices and emergency departments. |
|
|
64. MOA of BZDs?
|
a. Potentiate the effects of GABA by ↑ the frequency of chloride channel opening.
|
|
|
63. BZDs?
|
a. Commonly used in tx of anxiety disorders.
b. Easily obtained via prescription from physician offices and emergency departments. |
|
|
63. BZDs?
|
a. Commonly used in tx of anxiety disorders.
b. Easily obtained via prescription from physician offices and emergency departments. |
|
|
63. BZDs?
|
a. Commonly used in tx of anxiety disorders.
b. Easily obtained via prescription from physician offices and emergency departments. |
|
|
65. Use of Barbiturates?
|
a. Used in the tx of epilepsy and as anaesthetics.
b. Potentiate the effects of GABA by ↑ the duration of chloride channel opening. c. At high doses, barbiturates act as direct GABA agonists and have a lower margin of safety relative to BZDs. |
|
|
64. MOA of BZDs?
|
a. Potentiate the effects of GABA by ↑ the frequency of chloride channel opening.
|
|
|
64. MOA of BZDs?
|
a. Potentiate the effects of GABA by ↑ the frequency of chloride channel opening.
|
|
|
64. MOA of BZDs?
|
a. Potentiate the effects of GABA by ↑ the frequency of chloride channel opening.
|
|
|
66. Synergism of barbiturates?
|
a. They are synergistic in combination w/BZDs and barbiturates (as well as other CNS depressants).
b. Respiratory depression can occur as a complication. |
|
|
65. Use of Barbiturates?
|
a. Used in the tx of epilepsy and as anaesthetics.
b. Potentiate the effects of GABA by ↑ the duration of chloride channel opening. c. At high doses, barbiturates act as direct GABA agonists and have a lower margin of safety relative to BZDs. |
|
|
65. Use of Barbiturates?
|
a. Used in the tx of epilepsy and as anaesthetics.
b. Potentiate the effects of GABA by ↑ the duration of chloride channel opening. c. At high doses, barbiturates act as direct GABA agonists and have a lower margin of safety relative to BZDs. |
|
|
65. Use of Barbiturates?
|
a. Used in the tx of epilepsy and as anaesthetics.
b. Potentiate the effects of GABA by ↑ the duration of chloride channel opening. c. At high doses, barbiturates act as direct GABA agonists and have a lower margin of safety relative to BZDs. |
|
|
67. Intoxication w/sedative hypnotics?
|
a. Drowsiness/confusion.
b. Hypotension c. Slurred speech d. Incoordination e. Ataxia f. Mood lability g. Impaired judgement h. Nystagmus i. Respiratory depression j. Coma or death in overdose. |
|
|
66. Synergism of barbiturates?
|
a. They are synergistic in combination w/BZDs and barbiturates (as well as other CNS depressants).
b. Respiratory depression can occur as a complication. |
|
|
66. Synergism of barbiturates?
|
a. They are synergistic in combination w/BZDs and barbiturates (as well as other CNS depressants).
b. Respiratory depression can occur as a complication. |
|
|
66. Synergism of barbiturates?
|
a. They are synergistic in combination w/BZDs and barbiturates (as well as other CNS depressants).
b. Respiratory depression can occur as a complication. |
|
|
67. Intoxication w/sedative hypnotics?
|
a. Drowsiness/confusion.
b. Hypotension c. Slurred speech d. Incoordination e. Ataxia f. Mood lability g. Impaired judgement h. Nystagmus i. Respiratory depression j. Coma or death in overdose. |
|
|
67. Intoxication w/sedative hypnotics?
|
a. Drowsiness/confusion.
b. Hypotension c. Slurred speech d. Incoordination e. Ataxia f. Mood lability g. Impaired judgement h. Nystagmus i. Respiratory depression j. Coma or death in overdose. |
|
|
67. Intoxication w/sedative hypnotics?
|
a. Drowsiness/confusion.
b. Hypotension c. Slurred speech d. Incoordination e. Ataxia f. Mood lability g. Impaired judgement h. Nystagmus i. Respiratory depression j. Coma or death in overdose. |
|
|
68. Tx of sedative-hypnotic intoxication?
|
a. Maintain airway, breathing, and circulation. Monitor vital signs.
b. Activated charcoal and gastric lavage to prevent further GI absorption (if drug was ingested in the prior 4-6 hrs). |
|
|
68. Tx of sedative-hypnotic intoxication?
|
a. Maintain airway, breathing, and circulation. Monitor vital signs.
b. Activated charcoal and gastric lavage to prevent further GI absorption (if drug was ingested in the prior 4-6 hrs). |
|
|
68. Tx of sedative-hypnotic intoxication?
|
a. Maintain airway, breathing, and circulation. Monitor vital signs.
b. Activated charcoal and gastric lavage to prevent further GI absorption (if drug was ingested in the prior 4-6 hrs). |
|
|
68. Tx of sedative-hypnotic intoxication?
|
a. Maintain airway, breathing, and circulation. Monitor vital signs.
b. Activated charcoal and gastric lavage to prevent further GI absorption (if drug was ingested in the prior 4-6 hrs). |
|
|
69. Tx for barbiturates ONLY?
|
a. Alkalinize urine w/sodium bicarbonate to promote renal excretion.
|
|
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69. Tx for barbiturates ONLY?
|
a. Alkalinize urine w/sodium bicarbonate to promote renal excretion.
|
|
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69. Tx for barbiturates ONLY?
|
a. Alkalinize urine w/sodium bicarbonate to promote renal excretion.
|
|
|
69. Tx for barbiturates ONLY?
|
a. Alkalinize urine w/sodium bicarbonate to promote renal excretion.
|
|
|
70. Tx for BZDs only?
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a. Flumazenil in overdose.
|
|
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70. Tx for BZDs only?
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a. Flumazenil in overdose.
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70. Tx for BZDs only?
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a. Flumazenil in overdose.
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70. Tx for BZDs only?
|
a. Flumazenil in overdose.
|
|
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71. Sedative-hypnotic withdrawal?
|
a. Abrupt abstinence after chronic use can be life threatening.
b. While physiological dependence is more likely w/short-acting agents, longer-acting agents can also cause dependence and withdrawal sx. |
|
|
71. Sedative-hypnotic withdrawal?
|
a. Abrupt abstinence after chronic use can be life threatening.
b. While physiological dependence is more likely w/short-acting agents, longer-acting agents can also cause dependence and withdrawal sx. |
|
|
71. Sedative-hypnotic withdrawal?
|
a. Abrupt abstinence after chronic use can be life threatening.
b. While physiological dependence is more likely w/short-acting agents, longer-acting agents can also cause dependence and withdrawal sx. |
|
|
72. GHB?
|
a. GHB is a dose-specific CNS depressant that produces memory loss, respiratory distress, and coma.
b. It is commonly used as a date-rape drug. |
|
|
71. Sedative-hypnotic withdrawal?
|
a. Abrupt abstinence after chronic use can be life threatening.
b. While physiological dependence is more likely w/short-acting agents, longer-acting agents can also cause dependence and withdrawal sx. |
|
|
72. GHB?
|
a. GHB is a dose-specific CNS depressant that produces memory loss, respiratory distress, and coma.
b. It is commonly used as a date-rape drug. |
|
|
72. GHB?
|
a. GHB is a dose-specific CNS depressant that produces memory loss, respiratory distress, and coma.
b. It is commonly used as a date-rape drug. |
|
|
72. GHB?
|
a. GHB is a dose-specific CNS depressant that produces memory loss, respiratory distress, and coma.
b. It is commonly used as a date-rape drug. |
|
|
73. What type of drug withdrawal has the highest mortality rate?
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a. Barbiturate withdrawal.
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74. Flumazenil MOA?
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a. Flumazenil is a very short-acting BZD antagonist used for treating BZD overdose.
b. Use with caution when treating overdose, as it may precipitate seizures. |
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75. Treatment of choice for opiate overdose!?!?
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a. Naloxone.
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76. Note: In general, withdrawal from drugs that are sedating is life threatening, while withdrawal from stimulants is not.
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76. Note: In general, withdrawal from drugs that are sedating is life threatening, while withdrawal from stimulants is not.
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77. Tx of sedative withdrawal?
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a. BZD taper
b. Carbamazepine (Tegretol) or valproic acid (Depakote) may be used for seizure prevention. |
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78. What opioid is a common ingredient in cough syrup?
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a. Dextromethorphan.
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79. What 2 groups of receptors are stimulated by opioids?
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a. Opiate receptors (mu, kappa, and delta), which are normally stimulated by endogenous opiates and are involves in analgesia, sedation, and dependence.
b. Opioids also have effects on the dopaminergic system, which mediates their addictive and rewarding properties. |
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80. What are the most commonly abused opioids?
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a. Prescription opioids:
1. OxyContin (oxycodone) 2. Vicodin (hydrocodone/acetaminophen) 3. Percocet (oxycodone/acetaminophen) 4. Not heroin. |
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81. Most common cause of death from street heroin usage?
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a. Infection secondary to needle sharing.
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82. Clinical presentation of opioid intoxication?
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a. Drowsiness
b. N/V c. Constipation! d. Slurred speech e. Constricted Pupils!!! f. Seizures g. Respiratory depression, which may progress to coma or death in overdose. |
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83. What drugs, taken w/opioids may cause serotonin syndrome?
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a. Meperidine and MAOIs.
i. i.e. Hyperthermia, confusion, hyper or hypotension, and muscular rigidity. |
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84. Tx of opioid abuse?
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a. ABCs
b. In overdose: Naloxone or naltrexone (opioid antagonists) will improve respiratory depression by may cause severe withdrawal in an opioid-dependent pt. |
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85. Classic triad of opioid overdose?
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1. Respiratory depression
2. Altered mental status 3. Miosis. |
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86. Why is Meperidine the exception to the opioids?
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a. Bc it dilates pupils.
b. “Demerol Dilates pupils”. |
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87. Opiate intoxication sx?
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a. N/V
b. Sedation c. ↓ Pain d. ↓ GI motility e. Pupil constriction. f. Respiratory depression. |
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88. Opiate withdrawal?
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a. Not life threatening but abstinence syndrome in the opioid-dependent person -> unpleasant withdrawal syndrome characterized by dysphoria, insomnia, lacrimation, rhinorrhea, yawning, weakness, sweating, piloerection, N/V
b. Fever. c. Dilated pupils d. Abdominal cramps e. Arthralgia, myalgia f. HTN, Tachycardia g. Craving. |
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89. Tx of Opiate withdrawal for moderate sx?
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a. Symptomatic tx w/clonidine (for autonomic signs and sx of withdrawal)
b. NSAIDs for pain c. Dicyclomine for abdominal cramps, etc. |
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90. Tx of Opiate withdrawal for severe sx?
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a. Detox w/buprenorphine or methadone.
b. Monitor degree of withdrawal w/COWS (clinical Opioid Withdrawal Scale), which uses objective measures (ie, pulse, pupil size, tremor) to assess withdrawal severity. |
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91. Rapid recovery of consciousness following IV naloxone (opiod antagonist) is consistent with?
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a. Opioid overdose.
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