Psychiatry Clerkship_3 Flashcards

1
Q

the earliest symptoms of etoh withdrawal begin when ?

A

6-24h after patient’s last drink and depend on the duration and quantity of etoh consumption

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2
Q

when do seizures occur in alcohol withdrawal?

A

generalized tonic clonic seizures usually occur between 6-48h after cessation of drinking, with a peak around 13-24h

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3
Q

what fraction of etoh withdrawal patients with seizures develop DTs?

A

03-Jan

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4
Q

what electrolyte imbalance can predispose to seizures in etoh withdrawal?

A

hypomagnesemia

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5
Q

seizures in alcohol withdrawal are treated with what?

A

benzos, NOT anticonvulsants

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6
Q

EtOH withdrawal symptoms usually begin in how long?

A

6-24h

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7
Q

EtOH withdrawal symptoms typically last how long?

A

2-7 days

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8
Q

what are the mild EtOH withdrawal symptoms?

A

irritability • tremor • insomnia

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9
Q

what are the moderate EtOH withdrawal symptoms?

A

diaphoresis • hypertension • tachycardia • fever • disorientation

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10
Q

what are the severe symptoms of EtOH withdrawal?

A

tonic-clonic seizures • DT’s • hallucinations

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11
Q

delirium tremens carries what percent risk of mortality?

A

15-25%

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12
Q

what percent of patients hospitalized for EtOH withdrawal get DTs?

A

5%

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13
Q

what is the most serious form of EtOH withdrawal

A

DT’s

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14
Q

when do DT’s occur?

A

usually begins within 48-72h post last drink but may occur later (90% of cases within 7 days)

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15
Q

what predisposes to DT’s?

A

physical illness

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16
Q

in addition to delirium, symptoms of DT’s may include what?

A

hallucinations (MC visual) • gross tremor • autonomic instability • fluctuating levels of psychomotor activity

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17
Q

what is the treatment for delirium tremens?

A
  • benzodiazepines (chlordiazepoxide, diazepam, lorazepam) should be given in sufficient doses to keep the patient calm and lightly sedated then tapered down slowly [or depakote/tegretol taper] • - antipsychotics and temporary restraints for severe agitation • - thiamine,folic acid, and a multivitamin to treat nutritional deficiencies • - correct lytes and fluids • - monitor CIWA scale • - watch level of consciousness and watch for trauma • - check for hepatic failure
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18
Q

how many positives constitutes a positive CAGE questionnaire?

A

2

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19
Q

at risk or heavy drinking for men is how many drinks?

A

> 4/d or >14/wk

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20
Q

at risk or heavy drinking for women is how many drinks?

A

> 3/d or >7/wk

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21
Q

what are the biochemical markers used to monitor drinking?

A

BAL • LFT’s • GGT • CDT • MCV

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22
Q

AST:ALT ratio >2:1 and elevated CGT suggest what?

A

excessive alcohol use

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23
Q

what is the effect of alcohol on LFTs and MCV?

A

↑LFTs • ↑MCV

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24
Q

what are the medications for alcohol dependence?

A
  1. disulfiram (antabuse) • 2. naltrexone (revia, IM-vivitrol) • 3. acamprosate (campral) • 4. topiramate (topamax)
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25
Q

MOA of disulfiram?

A

blocks aldehyde dehydrogenase in the liver

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26
Q

disulfiram is contraindicated in what?

A

severe cardiac disease, pregnancy, psychosis

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27
Q

disulfiram is best used in whom?

A

highly motivated patients, as medication adherence is an issue

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28
Q

what is the MOA of naltrexone?

A

opioid receptor blocker • - works by ↓ desire/craving and high associated with EtOH

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29
Q

greater benefit for naltrexone use is seen in whom?

A

patients with family history of alcoholism

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30
Q

what will happen if you give naltrexone to a patient with opioid dependence?

A

precipitates withdrawal

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31
Q

what is the MOA of acamprosate?

A

structurally similar to GABA, thought to inhibit the glutaminergic system

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32
Q

how should acamprosate be used?

A

should be started postdetoxification for relapse prevention in patients who have stopped drinking

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33
Q

what is the major advantage of acamprosate?

A

can be used in patients with liver disease

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34
Q

acamprosate is contraindicated in who?

A

severe renal disease

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35
Q

what is the MOA of topiramate?

A

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

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36
Q

what are the long term psychiatric complications of alcohol intake?

A

wernicke’s encephalopathy → korsakoff syndrome

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37
Q

wernicke’s encephalopathy is caused by what?

A

caused by thiamine (B1) deficiency resulting from poor nutrition

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38
Q

what is the course and prognosis of wernicke’s encephalopathy?

A

acute and can be reversed with thiamine therapy

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39
Q

what are the features of wernicke’s encephalopathy?

A

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

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40
Q

what is the course of korsakoff syndrome?

A

reversible in only 20% of patients

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41
Q

what is the MOA of cocaine?

A

cocaine blocks dopamine reuptake from the synaptic cleft, causing a stimulant effect • - dopamine plays a role in behavioral reinforcement (reward system)

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42
Q

what are the general effects of cocaine intoxication?

A

euphoria, heightened self-esteem, ↑/↓ BP, tachy/bradycardia, nausea, dilated pupils, weight loss, psychomotor agitation or depression, chills, and sweating

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43
Q

what are the dangerous effects of cocaine intoxication?

A

respiratory depression, seizures, arrhythmias, paranoia, and hallucinations (especially tactile). since cocaine is an indirect sympathomimetic, intoxication mimics the fight or flight response

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44
Q

what are the deadly effects of cocaine intoxication?

A

cocaine’s vasoconstrictive effect may result in MI or stroke

45
Q

cocaine overdose can cause death secondary to what?

A

cardiac arrhythmia • MI • seizure • respiratory depression

46
Q

what is the management for mild to moderate agitation and anxiety due to cocaine?

A

reassurance of the patient and benzodiazepines

47
Q

what is the treatment for severe agitation or psychosis due to cocaine?

A

antipsychotics (haloperidol)

48
Q

what is the symptomatic support for cocaine intoxication?

A

control hypertension • arrhythmias

49
Q

what do you do for a cocaine intoxicated patient whose temp is >102F?

A

it is a medical emergency and should be treated aggressively with ice bath, cooling blanket, and other supportive measures

50
Q

treatment for cocaine withdrawal includes what?

A
  • there is no FDA approved pharmacotherapy for cocaine dependence • - off label meds are sometimes used (disulfiram, aripiprazole) • - psychological interventions (contingency management, group therapy) are efficacious and are mainstay treatment
51
Q

is abrupt abstinence of cocaine life threatening?

A

no

52
Q

with respect to cocaine use, what is postintoxication depression?

A

crash: • malaise, fatigue, hypersomnolence, depression, hunger, constricted pupils, vivid dreams, psychomotor agitation or retardation- occaisonal suicidality

53
Q

with mild to moderate cocaine use, withdrawal symptoms resolve when?

A

within 18 hours

54
Q

with heavy, chronic cocaine use, withdrawal symptoms last how long?

A

may last for weeks, but usually peak in several days

55
Q

what is the management for cocaine withdrawal?

A

treatment is supportive, but severe psychotic symptoms may warrant hospitalization

56
Q

what is the MOA of classic amphetamines?

A

block reuptake and facilitate release of dopamine and norepinephrine from nerve endings, causing a stimulant effect

57
Q

what are some examples of classic amphetamines?

A

dextroamphetamine (dexedrine) • methylphenidate (ritalin) • methamphetamine (desoxyn, ice, speed, crystal meth, crank)

58
Q

heavy use of amphetamines can cause what?

A

amphetamine psychosis, a psychotic state that may mimic schizophrenia

59
Q

what are the symptoms of amphetamine abuse?

A

dialted pupils, ↑ libido, perspiration, respiratory depression, chest pain

60
Q

chronic amphetamine use can lead to what?

A

acne and accelerated tooth decay (meth mouth)

61
Q

amphetamines are used medically in the treatment of what?

A

narcolepsy • ADHD • depressive disorders

62
Q

what is the MOA of substituted “designer” amphetamines?

A

release dopamine, norepinephrine, sertonin from nerve endings

63
Q

what are some exampled of substituted amphetamines?

A

MDMA, MDEA

64
Q

substituted amphetamine use is associated with which situations?

A

dance clubs and raves

65
Q

what can you get if you take substituted amphetamines with SSRI’s?

A

serotonin syndrome

66
Q

what are some of the possible consequences of amphetamine use?

A

↑ tolerance • can also → seizures

67
Q

amphetamine overdose can → what?

A

hyperthermia, dehydration, rhabdomyolysis → renal failure

68
Q

amphetamine withdrawal can → ?

A

prolonged depression; occaisionally complications of their long half life can cause psychosis

69
Q

what is the treatment for amphetamine intoxication?

A

rehydrate, correct electrolyte balance, and treat hyperthermia

70
Q

Ketamine can produce which effects?

A

tachycardia, tachypnea, hallucinations, amnesia

71
Q

what is the mnemonic for PCP intoxication symptoms?

A

RED DANES • Rage • Erythema • Dilated pupils • Delusions • Amnesia • Nystagmus • Excitation • Skin dryness

72
Q

what is the MOA of PCP?

A

a dissociative, hallucinogenic that antagonizes NMDA glutamate receptors and activates dopaminergic neurons. can have stimulant or depressant effects depending on the dose

73
Q

what is the clinical presentation of PCP intoxication?

A

agitation • depersonalization • hallucinations • synesthesia • impaired judgement • memory impairment • assaultiveness • nystagmus • ataxia • dysarthria • hypertension, • tachycardia • muscle rigidity • high tolerance to pain

74
Q

overdose of PCP can cause what?

A

seizures, coma, death

75
Q

what are the types of nystagmus seen in PCP intoxication?

A

rotary, horizontal, vertical

76
Q

which type of nystagmus is pathognomonic for PCP intoxication?

A

rotary

77
Q

what is the treatment for PCP intoxication?

A
  • monitor vitals, lytes, minimize sensory stimulation • - use benzos (lorazepam) to treat agitation, anxiety, muscle spasms, seizures • - use antipsychotics (haldol) to control severe agitation or psychotic symptoms
78
Q

which types of hallucinations are seen in both cocaine and PCP abuse?

A

tactile and visual

79
Q

more than with other drugs, intoxication with what leads to violence?

A

PCP

80
Q

what are the symptoms of PCP withdrawal?

A

no withdrawal syndrome, but flashbacks may occur

81
Q

agents in the sedative-hypnotics category category include what?

A

BDZ’s • barbiturates • zolpidem • zaleplon • GHB • meprobamate

82
Q

MOA of BDZ’s?

A

potentiate the effects of GABA by ↑ the frequency of chloride channel opening

83
Q

MOA of barbiturates?

A

potentiate the effects of GABA by ↑ the duration of chloride channel opening

84
Q

which are more dangerous, barbiturates or BDZ’s?

A

at high doses, barbiturates act as direct GABA agonists and have a lower margin of safety than BDZ’s

85
Q

What is GHB?

A

a dose specific CNS depressant that produces memory loss, respiratory distress, and coma. it is commonly used as a date rape drug

86
Q

of all the types of withdrawals, withdrawal from what has the highest mortality rate?

A

barbiturates

87
Q

intoxication with sedatives produces what?

A

drowsiness • confusion • hypotension • slurred speech • incoordination • ataxia • mood lability • impaired judgement • nystagmus • respiratory depression • coma • death

88
Q

symptoms of sedative-hypnotics intoxication are synergistic when?

A

when combined with EtOH or opioids/narcotics

89
Q

long term sedative use may → ?

A

dependence and may cause depressive symptoms

90
Q

what is flumazenil?

A

a very short acting BDZ antagonist used for treating BDZ overdose

91
Q

why should flumazenil be used with caution?

A

when treating overdose, it may precipitate seizures

92
Q

what is the treatment for sedative-hypnotic intoxication

A
  • maintain airway, breathing, circulation. montior VS • - activated charcoal and gastric lavage to prevent further absorption if drug ingested in prior 4-6h • - supportive care- improve respiratory status, control hypotension
93
Q

what is the treatment specific to barbiturate intoxication?

A

alkalinize urine with sodium bicarbonate to promote renal excretion

94
Q

what is the treatment specific to BDZ intoxication?

A

flumazenil in overdose

95
Q

what is the treatment of choice for opiate overdose?

A

naloxone

96
Q

what is the treatment for sedative-hypnotic withdrawal?

A

BDZ taper • carbamazepine or depakote taper may be used for seizure prevention

97
Q

what is the most common cause of death from street heroin usage?

A

infection secondary to needle sharing

98
Q

what is the MOA of opioids?

A

stimulate opiate receptors (μ, κ, δ) which are normally stimulated by endogenous opiates and are involved in analgesia, sedation, dependence

99
Q

examples of opioids include what?

A

heroin • oxycodone • codeine • DXM • morphine • methadone • meperidine

100
Q

what are the most commonly abused opioids?

A

oxycontin • vicodin • percocet • NOT heroin

101
Q

what behaviors should alert a physician to opioid misuse?

A

losing medication • doctor shopping • running out of meds early

102
Q

opioid intoxication causes what?

A

drowsiness • nausea/vomting • constipation • slurred speech • constricted pupils • seizures • respiratory depression • may → coma or death in overdose

103
Q

what is the exception to opioids producing miosis?

A

Demerol Dilates pupils

104
Q

which opioid is known to cause serotonin syndrome?

A

meperidine and MAOI together

105
Q

what is the treatment for opiate intoxication?

A
  • ensure adequate airway, breathing, circulation • - in overdose, administration of naloxone or naltrexone will improve respiratory depression but may cause severe withdrawal in an opioid-dependent patient • - ventilatory support may be required
106
Q

what is the classic triad of opioid overdose?

A

Rebels Admire Morphine • Respiratory depression • Altered mental status • Miosis

107
Q

can eating poppy seed bagels or muffins result in a urine drug screen that is positive for opioids?

A

yes

108
Q

is opiate withdrawal deadly?

A

no

109
Q

abstinence in the opioid-dependent individual →?

A

unpleasant withdrawal syndrome characterized by dysphoria, insomnia, lacrimation, rhinorrhea, yawning, weakness, sweating, piloerection, N/V, fever, dilated pupils, abdominal cramps, arthralgia, myalgia, hypertension, tachycardia, craving