Alcohol and seditive abuse Flashcards
1. Describe the impact of alcohol and sedative/hypnotic use on individuals and society 2. Analyze a clinical scenario and choose the correct treatment for alcohol and sedative/hypnotic withdrawal 3. Analyze a clinical scenario and choose the correct treatment for alcohol dependence
def of binge drinking
4 (women)/5 (men) drinks in one occasion
def of heavy drinking
1(women)/2( men) drinks a day on average
are most binge drinkers Et OH dependant
no
% of men/women who will meet criteria for EtOH dependance at some point in their lives
17 men/8% women
most common drug in ED misuse/abuse cases
benzos
gender most likely to have sedative abuse
women
usually fatal BAC
.5
sedatives with respiratory compromise by themselves
barbos
what must be given before glucose in an ER setting
thiamine
why must thiamine must be given before glucose in ER
prevent wernicke’s
pathology of wernicke-korsakoff’s
atrophy of mammillary bodies/thalmus
sx of wernickes
confusion, 3/4 CN lesion signs, ataxia, coma/death
sx of korsakoff’s
amnesia, confabulation, hallucinations
NT acted upon by EtOH
GABAA, glutamate
why do you “black out” when drunk
decrease in glu functioning on NMDA receptors
heritibility rate of EtOH dependance
50%
predictors of EtOH withdrawal severity
older age lenght/severity of habit prior withdrawal (kindling) major med/surg problems sedative/hypnotic use
lab value to identify heavy drinkers
CDT
time frame for DT’s
72-105hours
when do AW seizures occur
24-48 hours
DT sx
marked autonomic arousal
shakes, sweats, HTN, tachycardia
delerium
drugs that can cause fatal withdrawal
EtOH, benzo, barbo
treatment for Acute AW
benzo
reasons for useing long t 1/2 benzo in AW
less seziures. smoother detox
long t 1/2 benzos for AW
chlordiazepoxide, diazepam
why would you use short t 1/2 benzo for AW
less oversedation, safer in elderly or with liver damage
short t 1/2 benzo
lorazepam, oxazepam
used to determine AW severity
CIWA
the “make you sick” anti EtOH drug
disulfiram
SE of disulfram
drowsy, fatigue, exacerbate psychosis/depression
SE of naltrexone
liver damage, flu-like sx
SE of acamprosate
dirrhea, bloating, rash
MOA of disulfram
inhibits aldehyde dehygrongenase to allow unpleasant acetaldehyde accumulation
acamprosate MOA
modulates activity of glu
naltrexone MOA
modulates activity of endogenous opioids
