Psychiatry Clerkship_3 Flashcards
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?
03-Jan
what electrolyte imbalance can predispose to seizures in etoh withdrawal?
hypomagnesemia
seizures in alcohol withdrawal are treated with what?
benzos, NOT anticonvulsants
EtOH withdrawal symptoms usually begin in how long?
6-24h
EtOH withdrawal symptoms typically last how long?
2-7 days
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?
15-25%
what percent of patients hospitalized for EtOH withdrawal get DTs?
5%
what is the most serious form of EtOH withdrawal
DT’s
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?
physical illness
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?
2
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?
- 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?
precipitates withdrawal
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