Flashcards in Psychiatry Clerkship_3 Deck (109):
the earliest symptoms of etoh withdrawal begin when ?
6-24h after patient's last drink and depend on the duration and quantity of etoh consumption
when do seizures occur in alcohol withdrawal?
generalized tonic clonic seizures usually occur between 6-48h after cessation of drinking, with a peak around 13-24h
what fraction of etoh withdrawal patients with seizures develop DTs?
what electrolyte imbalance can predispose to seizures in etoh withdrawal?
seizures in alcohol withdrawal are treated with what?
benzos, NOT anticonvulsants
EtOH withdrawal symptoms usually begin in how long?
EtOH withdrawal symptoms typically last how long?
what are the mild EtOH withdrawal symptoms?
irritability • tremor • insomnia
what are the moderate EtOH withdrawal symptoms?
diaphoresis • hypertension • tachycardia • fever • disorientation
what are the severe symptoms of EtOH withdrawal?
tonic-clonic seizures • DT's • hallucinations
delirium tremens carries what percent risk of mortality?
what percent of patients hospitalized for EtOH withdrawal get DTs?
what is the most serious form of EtOH withdrawal
when do DT's occur?
usually begins within 48-72h post last drink but may occur later (90% of cases within 7 days)
what predisposes to DT's?
in addition to delirium, symptoms of DT's may include what?
hallucinations (MC visual) • gross tremor • autonomic instability • fluctuating levels of psychomotor activity
what is the treatment for delirium tremens?
- 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
how many positives constitutes a positive CAGE questionnaire?
at risk or heavy drinking for men is how many drinks?
>4/d or >14/wk
at risk or heavy drinking for women is how many drinks?
>3/d or >7/wk
what are the biochemical markers used to monitor drinking?
BAL • LFT's • GGT • CDT • MCV
AST:ALT ratio >2:1 and elevated CGT suggest what?
excessive alcohol use
what is the effect of alcohol on LFTs and MCV?
↑LFTs • ↑MCV
what are the medications for alcohol dependence?
1. disulfiram (antabuse) • 2. naltrexone (revia, IM-vivitrol) • 3. acamprosate (campral) • 4. topiramate (topamax)
MOA of disulfiram?
blocks aldehyde dehydrogenase in the liver
disulfiram is contraindicated in what?
severe cardiac disease, pregnancy, psychosis
disulfiram is best used in whom?
highly motivated patients, as medication adherence is an issue
what is the MOA of naltrexone?
opioid receptor blocker • - works by ↓ desire/craving and high associated with EtOH
greater benefit for naltrexone use is seen in whom?
patients with family history of alcoholism
what will happen if you give naltrexone to a patient with opioid dependence?
what is the MOA of acamprosate?
structurally similar to GABA, thought to inhibit the glutaminergic system
how should acamprosate be used?
should be started postdetoxification for relapse prevention in patients who have stopped drinking
what is the major advantage of acamprosate?
can be used in patients with liver disease
acamprosate is contraindicated in who?
severe renal disease
what is the MOA of topiramate?
anticonvulsant that potentiates GABA and inhibits glutamate receptors • - reduces cravings for alcohol
what are the long term psychiatric complications of alcohol intake?
wernicke's encephalopathy → korsakoff syndrome
wernicke's encephalopathy is caused by what?
caused by thiamine (B1) deficiency resulting from poor nutrition
what is the course and prognosis of wernicke's encephalopathy?
acute and can be reversed with thiamine therapy
what are the features of wernicke's encephalopathy?
ataxia • confusion • ocular abnormalities (nystagmus, gaze palsies)
what is the course of korsakoff syndrome?
reversible in only 20% of patients
what is the MOA of cocaine?
cocaine blocks dopamine reuptake from the synaptic cleft, causing a stimulant effect • - dopamine plays a role in behavioral reinforcement (reward system)
what are the general effects of cocaine intoxication?
euphoria, heightened self-esteem, ↑/↓ BP, tachy/bradycardia, nausea, dilated pupils, weight loss, psychomotor agitation or depression, chills, and sweating
what are the dangerous effects of cocaine intoxication?
respiratory depression, seizures, arrhythmias, paranoia, and hallucinations (especially tactile). since cocaine is an indirect sympathomimetic, intoxication mimics the fight or flight response
what are the deadly effects of cocaine intoxication?
cocaine's vasoconstrictive effect may result in MI or stroke
cocaine overdose can cause death secondary to what?
cardiac arrhythmia • MI • seizure • respiratory depression
what is the management for mild to moderate agitation and anxiety due to cocaine?
reassurance of the patient and benzodiazepines
what is the treatment for severe agitation or psychosis due to cocaine?
what is the symptomatic support for cocaine intoxication?
control hypertension • arrhythmias
what do you do for a cocaine intoxicated patient whose temp is >102F?
it is a medical emergency and should be treated aggressively with ice bath, cooling blanket, and other supportive measures
treatment for cocaine withdrawal includes what?
- 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
is abrupt abstinence of cocaine life threatening?
with respect to cocaine use, what is postintoxication depression?
crash: • malaise, fatigue, hypersomnolence, depression, hunger, constricted pupils, vivid dreams, psychomotor agitation or retardation- occaisonal suicidality
with mild to moderate cocaine use, withdrawal symptoms resolve when?
within 18 hours
with heavy, chronic cocaine use, withdrawal symptoms last how long?
may last for weeks, but usually peak in several days
what is the management for cocaine withdrawal?
treatment is supportive, but severe psychotic symptoms may warrant hospitalization
what is the MOA of classic amphetamines?
block reuptake and facilitate release of dopamine and norepinephrine from nerve endings, causing a stimulant effect
what are some examples of classic amphetamines?
dextroamphetamine (dexedrine) • methylphenidate (ritalin) • methamphetamine (desoxyn, ice, speed, crystal meth, crank)
heavy use of amphetamines can cause what?
amphetamine psychosis, a psychotic state that may mimic schizophrenia
what are the symptoms of amphetamine abuse?
dialted pupils, ↑ libido, perspiration, respiratory depression, chest pain
chronic amphetamine use can lead to what?
acne and accelerated tooth decay (meth mouth)
amphetamines are used medically in the treatment of what?
narcolepsy • ADHD • depressive disorders
what is the MOA of substituted "designer" amphetamines?
release dopamine, norepinephrine, sertonin from nerve endings
what are some exampled of substituted amphetamines?
substituted amphetamine use is associated with which situations?
dance clubs and raves
what can you get if you take substituted amphetamines with SSRI's?
what are some of the possible consequences of amphetamine use?
↑ tolerance • can also → seizures
amphetamine overdose can → what?
hyperthermia, dehydration, rhabdomyolysis → renal failure
amphetamine withdrawal can → ?
prolonged depression; occaisionally complications of their long half life can cause psychosis
what is the treatment for amphetamine intoxication?
rehydrate, correct electrolyte balance, and treat hyperthermia
Ketamine can produce which effects?
tachycardia, tachypnea, hallucinations, amnesia
what is the mnemonic for PCP intoxication symptoms?
RED DANES • Rage • Erythema • Dilated pupils • Delusions • Amnesia • Nystagmus • Excitation • Skin dryness
what is the MOA of PCP?
a dissociative, hallucinogenic that antagonizes NMDA glutamate receptors and activates dopaminergic neurons. can have stimulant or depressant effects depending on the dose
what is the clinical presentation of PCP intoxication?
agitation • depersonalization • hallucinations • synesthesia • impaired judgement • memory impairment • assaultiveness • nystagmus • ataxia • dysarthria • hypertension, • tachycardia • muscle rigidity • high tolerance to pain
overdose of PCP can cause what?
seizures, coma, death
what are the types of nystagmus seen in PCP intoxication?
rotary, horizontal, vertical
which type of nystagmus is pathognomonic for PCP intoxication?
what is the treatment for PCP intoxication?
- 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
which types of hallucinations are seen in both cocaine and PCP abuse?
tactile and visual
more than with other drugs, intoxication with what leads to violence?
what are the symptoms of PCP withdrawal?
no withdrawal syndrome, but flashbacks may occur
agents in the sedative-hypnotics category category include what?
BDZ's • barbiturates • zolpidem • zaleplon • GHB • meprobamate
MOA of BDZ's?
potentiate the effects of GABA by ↑ the frequency of chloride channel opening
MOA of barbiturates?
potentiate the effects of GABA by ↑ the duration of chloride channel opening
which are more dangerous, barbiturates or BDZ's?
at high doses, barbiturates act as direct GABA agonists and have a lower margin of safety than BDZ's
What is GHB?
a dose specific CNS depressant that produces memory loss, respiratory distress, and coma. it is commonly used as a date rape drug
of all the types of withdrawals, withdrawal from what has the highest mortality rate?
intoxication with sedatives produces what?
drowsiness • confusion • hypotension • slurred speech • incoordination • ataxia • mood lability • impaired judgement • nystagmus • respiratory depression • coma • death
symptoms of sedative-hypnotics intoxication are synergistic when?
when combined with EtOH or opioids/narcotics
long term sedative use may → ?
dependence and may cause depressive symptoms
what is flumazenil?
a very short acting BDZ antagonist used for treating BDZ overdose
why should flumazenil be used with caution?
when treating overdose, it may precipitate seizures
what is the treatment for sedative-hypnotic intoxication
- 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
what is the treatment specific to barbiturate intoxication?
alkalinize urine with sodium bicarbonate to promote renal excretion
what is the treatment specific to BDZ intoxication?
flumazenil in overdose
what is the treatment of choice for opiate overdose?
what is the treatment for sedative-hypnotic withdrawal?
BDZ taper • carbamazepine or depakote taper may be used for seizure prevention
what is the most common cause of death from street heroin usage?
infection secondary to needle sharing
what is the MOA of opioids?
stimulate opiate receptors (μ, κ, δ) which are normally stimulated by endogenous opiates and are involved in analgesia, sedation, dependence
examples of opioids include what?
heroin • oxycodone • codeine • DXM • morphine • methadone • meperidine
what are the most commonly abused opioids?
oxycontin • vicodin • percocet • NOT heroin
what behaviors should alert a physician to opioid misuse?
losing medication • doctor shopping • running out of meds early
opioid intoxication causes what?
drowsiness • nausea/vomting • constipation • slurred speech • constricted pupils • seizures • respiratory depression • may → coma or death in overdose
what is the exception to opioids producing miosis?
Demerol Dilates pupils
which opioid is known to cause serotonin syndrome?
meperidine and MAOI together
what is the treatment for opiate intoxication?
- 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
what is the classic triad of opioid overdose?
Rebels Admire Morphine • Respiratory depression • Altered mental status • Miosis
can eating poppy seed bagels or muffins result in a urine drug screen that is positive for opioids?
is opiate withdrawal deadly?