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psych substance related disorders Flashcards

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1
Q

abuse def

A

pattern of substance use that leads to impairment or distress for at least 12 mos with one or more of the following: failure to fulfill obligations at home or work, use in dangerous situations, recurrent substance related legal problems, continued use despite social or interpersonal problems due to the substance use

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2
Q

dependence def

A

substance use leading to impairment or distress manifested by at least three of the following in 12 mo period: tolerance, withdrawal,

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3
Q

cocaine use- how long is the urine drug screen pos for?

A

2-4 days

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4
Q

amphetamines- how long is the urine drug screen pos for?

A

3-4 days

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5
Q

PCP- how long is the urine drug screen pos for?

A

3-8 days

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6
Q

what lab values are elevated in PCP use?

A

CPK and AST

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7
Q

examples of sedative-hypnotics

A

barbiturates and benzos

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8
Q

short acting barbiturate

A

pentobarbitol; in your system for 24 hours

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9
Q

long acting barbiturate

A

phenobarbitol; stays in system for 3 weeks

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10
Q

short acting benzo

A

lorazepam; in your system for 3 days

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11
Q

long acting benzo

A

diazepam; in your system for 30 days

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12
Q

examples of opioids

A

methadone and oxycodon

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13
Q

urine drug test for opioids

A

pos for 2-3 days, depengind on the opioid used; methadone and oxycodon will come up neg on a general screen (must order separate panel)

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14
Q

urine drug test for marijuana

A

in heavy users, up to 4 weeks; after single use, about 3 days

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15
Q

what are the mechanisms of alcohol in the CNS?

A

activates GABA and serotonin; inhibits glutamate and voltage gated calcium channels; it is a potent CNS depressant

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16
Q

how is alcohol metabolized?

A

alcohol–>acetaldehyde–>acetic acid

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17
Q

enzyme that converts alc to acetaldehyde?

A

alcohol dehydrogenase

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18
Q

enzyme that converts acetaldehyde to acetic acid

A

aldehyde dehydrogenase

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19
Q

asians have less of what enzyme?

A

aldehyde dehydrogenase

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20
Q

the effects/BAL may be decreased if high tolerance has been developed

A

right

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21
Q

treatment for alcohol intox

A

ABC; thiamine and folate

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22
Q

when is GI evacuation indicated in alcohol poisoning

A

when a signif amount of alc was ingested in the past 30-60 mins

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23
Q

symptoms of alc withdrawal

A

insomnia, anxiety, diaphoresis, and tachycardia; anorexia, n/v, psychomotor agitation, fevers, seizures, hallucinations, and delirium

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24
Q

treatment for alc withdrawal

A

benzo taper (chlordiazepoxide (librium) is drug of choice); thiamine, folic acid, and multivitamin; correct electrolyte abnormalities; check for signs of hepatic failure

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25
Q

what can kill a person in alc withdrawal

A

seizures, htn, and arrythmias

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26
Q

when do the earliest signs of alc withdrawal occur?

A

6 to 24 hours after the patient’s last drink

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27
Q

seizures in alc withdrawal

A

between 6 and 48 hours after the patient’s last drink, with a peak around 13 to 24 hours

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28
Q

treatment for seizures in alc withdrawal>

A

benzos

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29
Q

alc withdrawal symptoms usually last how long?

A

2-7 days

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30
Q

when does delirium tremens begin?

A

48-72 hours after the last drink, but may occur later

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31
Q

mortality of DT if not treated

A

15 to 25%

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32
Q

symptoms of DT

A

delirium, visual hallucinations, gross tremor, autonomic instablity, and fluctuating levels of psychomotor activity

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33
Q

benzos

A

chlordiazepoxide, diazepam, or lorazepam

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34
Q

CAGE questionaire for alcohol abuse

A

have you ever wanted to cut down; have you ever felt annoyed by criticism of your drinking; have you ever felt guilty about drinking; have you taken a drink as eye opener

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35
Q

medications for alcohol dependence

A

disulfuram (antabuse); naltrexone (revia, IM-vivitrol); acamprosate (campral); topiramate (topamax)

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36
Q

disulfuram (anatabuse)

A

blocks aldehyde dehydrogenase and causes aversive reaction to alcohol; contraindic in cardiac disease, pregnancy, psychosis; need compliance

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37
Q

naltrexone

A

opioid receptor blocker; workse by decreasing the craving and high assoc with alc; in patients with opioid dependence, it will precipitate withdrawal

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38
Q

acamprosate

A

similar to GABA; inhibits the glutamatergic system; should be used for relapse preventation in patients who have stopped drinking; can be used in patients with liver disease; contraindic in renal disease patients

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39
Q

topiramate

A

anticonvulsant that potentiates GABA and inhibits glutamate receptors; reduces cravings for alcohol

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40
Q

features of wernicke’s encephalopathy

A

ataxia, confusion, ocular abnormalities (nystagmus, gaze palsies)

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41
Q

korsakoff syndrome

A

chronic amnestic syndrome, reversible in only 20% of patients; impaired recent memory, anterograde amnesia, compensatory confabulation

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42
Q

how does cocaine work?

A

blocks dopamine reuptake from the synaptic cleft; plays a role in the reward system of the brain

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43
Q

cocaine intoxication features

A

euphoria, heightened self-esteem; hypo or hypertension; tachycardia or bradycardia, nausea; dilated pupils (sympathetic!); chills and sweating

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44
Q

dangerous effects of cocaine

A

respiratory depression, seizures, arrhythmias, paranoia, hallucinations (esp tactile)

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45
Q

what is deadly about cocaine

A

vasoconstrictive effect may result in MI or stroke

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46
Q

management of cocaine intoxication

A

for mild or moderate, reassurance of patient or benzos; for severe agitation, antipsychotics (haldol); temp greater than 102 is a med emergency and should be treated withice bath, cooling blanket, and other supportive measures

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47
Q

treatment of cocaine dependence

A

no FDA approved drug; off label you can use disulfiram and ariprazole

48
Q

withdrawal from coke

A

not life threatening; produces crash (fatigue, hypersomnolence, depression, constricted pupils, hunger)

49
Q

how do amphetamines work

A

block reuptake and facilitate release of dopamine and norepi from nerve endings; causes a stimulant effect

50
Q

examples of amphetamines

A

dextroamphetamine (dexedrine); methylphenidate (ritalin); methamphetamine (“speed,” Desoxyn)

51
Q

what are amphetamines used for medically?

A

treatment of narcolepsy, ADHD, and depressive disorders

52
Q

what are the substituted (“designer”) amphetamines?

A

MDMA (ecstasy); MDEA (“eve”)

53
Q

what is different about the substituted amphetamines?

A

release dopamine, norepi, and serotonin; they have both hallucinogenic and stimulant properties; assoc with clubs and raves

54
Q

risk of serotonin syndrome with substituted amphetamiens

A

serotonin syndrome can occur if designer amphetamines are combined with SSRIs

55
Q

symptoms of amphetamine intoxication

A

similar to those of cocaine; MDMA and MDEA can induce a sense of closeness to others

56
Q

overdose of amphetamines

A

hyperthermia, dehydration, and rhabdomyolysis (leading to renal failure)

57
Q

amphetamine withdrawal

A

prolonged depression

58
Q

treatment for amphetamine intoxication

A

rehydrate, correct electrolyte imbalance, and treat hyperthermia

59
Q

mechanism of PCP

A

antagonizes NMDA glutamate receptors and activates dopaminergic neurons; can be stimulant or depressant depending on the dose

60
Q

relationship between ketamine and PCP

A

ketamine is less potent PCP

61
Q

date rate drug

A

ketamine; it is odorless and tasteless

62
Q

clinical presentation of PCP patient

A

agitation, depersonaliztion, hallucinations, synesthesia, impaired judgment, memory impairment, assaultiveness, nystagmus, ataxia, dysarthria, hypertension, tachycardia, muscle rigidity, and high tolerance to pain

63
Q

overdose of PCP

A

seizures, coma, and even death

64
Q

treatment for PCP

A

minimize sensory stimulation, benzos for agitation, anxiety, muscle spasms, and seizures; use antipsychotics for severe agitation or psychotic symptoms

65
Q

withdrawal from PCP

A

no withdrawal syndrome, but flashbacks (recurrence of intoxication symptoms due to release of the drug from lipid stores)

66
Q

sedative-hypnotic examples

A

benzos, barbiturates, zolpidem, zaleplon, GHB, meprobate, and others; these are highly abused

67
Q

how do benzos work?

A

potentiate GABA by increasing the freq of chloride channel opening

68
Q

when are barbiturates used?

A

treatment of epilepsy and as anesthetics

69
Q

mechanism of barbiturates

A

potentiate GABA by increasing the duration of chloride channel opening

70
Q

complication of too much barbiturates

A

respiratory depression

71
Q

intox with sedatives- symptoms

A

drowsiness, confusion, hypotension, slurred speech, incoordination, ataxia, mood lability, impaired judgment, nystagmus, resp depression, and coma or death in overdose

72
Q

long term sedative use

A

may lead to dependence and may cause depressive symptoms

73
Q

treatment for sedative intoxication

A

maintain ABC; use activated charcoal and gastric lavage to prevent further GI absorption (if drug was ingested in the prior 4-6 hours); supportive care

74
Q

treatment for barbiturate intox specifically

A

alkalinize urine with sodium bicarb to promote renal excretion

75
Q

treamtne for benzo intox

A

flumazenil in overdose

76
Q

physiologic dependence on sedatives is more likely in long or short acting?

A

short acting; but long acting agents can also cause dependence and withdrawal symptoms

77
Q

withdrawal symptoms from sedatives

A

same as from alcohol; worst sx in barbiturates

78
Q

treatment for sedative withdrawal

A

benzo taper; carbamazepine or valproic acid can be used for seizure prevention

79
Q

mechanism of opioids

A

stimulate opiate receptors (mu, kappa, and delta); involved in analgesiaa, sedation, and dependence

80
Q

examples of opiates

A

heroin, oxycodone, codeine, dextromethorphan, morphine, methadone, and meperidine (Demerol)

81
Q

major neurotransmitter involved with opioids

A

dopamine

82
Q

most commonly abused opiods

A

NOT heroin; actually the prescribed opioids like Vicodin, OxyContin, and percocet

83
Q

clinical presentation of opiate intoxication

A

drowsiness, n/v, constipation, constricted pupils (parasymp), seizures, and resp depression

84
Q

serotonin syndrome

A

can be seen when meperidine and MAOI are taken in combo; sx are hyperthermia, confusion, hyper or hypotension, and muscular rigidity

85
Q

treatment of opiod overdose

A

naloxone or naltrexone (opioid antagonists) will improve resp depression but may cause severe withdrawal in an opioid-dep patient

86
Q

withdrawl from opioids

A

not life-threatening; unpleasant syndrome characterized by dysphoria, insomnia, lacrimation, rhinorrhea, yawning, weakness, sweating, piloerection, n/v, fever, dilated pupuls

87
Q

treatment for opioid withdrawal

A

moderate sx can be treated with clonidine (for autonomic signs and sx of withdrawal), NSAIDs for prain, dicyclomine for abdominal cramps

88
Q

severe symptoms of opioid withdrawal- what is treatment?

A

detox wth buprenorphine or methadone

89
Q

three meds that treat opiod dependence

A

methadone, buprenorphine, naltrexone

90
Q

how does methadone work?

A

long-acting opioid receptor antag; administered once daily, signif reduces morbidity and mortality; gold standard for pregnant women

91
Q

buprenorphine

A

partial opioid receptor agonist; sublingual and safer than methadone; comes as Suboxone (buprenorphine plus naloxone)

92
Q

naltrexone

A

competitive opioid antagonist; precipitates withdrawal if used within 7 days of heroin use; compliance is an issue

93
Q

examples of hallucinogenic drugs of abuse

A

psilocybin (mushrooms); mescaline (peyote cactus), and LSD

94
Q

proposed mechanism for LSD

A

serotonergic systems

95
Q

physical dependence or withdrawal in hallucinogens?

A

no

96
Q

intoxication of hallucinogens; symptoms

A

perceptual changes; labile affect, dilated pupils, tachycardia, hypertension, hyperthermia, tremors, incoordination, sweating, and palpitations; usually lasts 6-12 hours but may last for days

97
Q

treatment for hallucinogens

A

monitor for dangerous behavior and reassure patient; use benzos and anti-psychotics if necessary for agitated psychoiss

98
Q

withdrawal symptoms from hallucinogens

A

none, but longterm LSD use may cause a patient to have flashbacks later in life

99
Q

how does marijauna work in the brain?

A

cannabinoid receptors in the brain inhibit adenylate cyclase

100
Q

benefits of marijuana

A

decrease nausea, increase appetite in AIDS patients, and derease intraocular pressure, muscle spasms, and tremor

101
Q

symptoms of marijuana

A

euphoria, anxiety, impaired motor coordination, perceptual disturbances, mild tachycardia, red eyes, dry mouth, and increased appetitie

102
Q

chronic marijuana use

A

resp problems like asthma and chronic bronchitis, suppression of immune system, and effects on reproductive hormones

103
Q

withdrawal from marijuana

A

irritability, anxiety, restlessnes, aggression, depression, strange dreams, headaches, sweating, insomnia, nausea, craving, and decr appetite

104
Q

mechanism of inhalents

A

CNS depressants

105
Q

examples of inhalents

A

solvents, glue, paint thinners, fuels, isobutyl nitrates (“huff,” “laughing gas,” “rush,” “bolt”)

106
Q

effects of inhalents

A

perceptual disturances, psychosis, lethargy, dizziness, n/c. headache, euphoria, hypoxia, cloudiness of consiousness, stupor, or coma

107
Q

acute intoxication of inhalents lasts how long?

A

minutes, stupor may last for hours

108
Q

overdose of inhalents

A

may be fatal secondary to resp depression or cardiac arrhythmias

109
Q

long term use of inhalents

A

permanent brain damage, peripheral nervous system, liver, kidney, heart and muscle

110
Q

treatment for inhlaent intoxication

A

ABCs; identify solvent because some (leaded gasoline) may require chelation

111
Q

mechanism of caffeine

A

adenosine antagonists causing increase cAMP and a stimulant effect via the dopaminergic system

112
Q

death by caffein

A

over 10 g (1000 cups); death may occur secondary to seizures and resp failure

113
Q

nicotine is addictive through actions on what neurotransmitter

A

dopamine

114
Q

Varenicline (chantix)

A

nicotinic cholinergic receptor partial agonist that mimics the action of nicotine and prevents withdrawal

115
Q

buproprion (zyban)

A

antidepressant that is also partial agonist at nACHR and inhib of dopamine reuptake; helps reduce withdrawal symptoms

116
Q

Nicotine replacement therapy

A

transdermal patch, gum, lozenge, nasal spray, and inhaler

Psych (23 decks)

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