AAD Flashcards
ALcoholism
chronic disease that when active, results in compulsive, out of control use of alcohol and neg. consequences
DSM 5
in the last yr have you
1. more than once tried to cut down drinking or tried and couldnt
2. spent a lot of time drinking or sick w after effects
3. wanted to drink so badly you couldnt think of anythign else
4. drinking interferes w taking care of home, family, job school
5. continued to drink even though in interfered w fam or friends
6. cut back on activities once important to you
7. more than once got into situation while drinking that inc chances of injury
8. continued to drink even though it was affecting mental health
9. have to drink more and more to get desired effect
10. withdrawal sx
2+ of these sx in past yr–> dx
DSM 5 and AUD severity
2-3 sx mild
4-5 mod
6+ severe
type I alcoholism
develops gradually over lifespan
equally prevalent in men and women
generally less severe health consequences
type II alcoholism
early onset
much more prevalent in men
more severe health consequences
AUD labs for dx
inc MCV
inc GGT
inc AST ALT (ALT x2 = AST)
inc uric acid, TG
ethyl glucuronide and ethyl sulfate
AAD most prevalent in which age group and sex
18-29 males
alcohol inhibits/simulates GABA-DA(inhibitory) and NMDA-glutamate(stimulatory) pathways?
stimulates GABA and inhibits NMDA
with time GABA down regulates and NMDA upregulates which precipitates withdrawal sx
“downreg the inhibitory and upreg the excitatory _ w/drawal = BAD”
alcohol and dopamine system
inc DA in mesolimbic system –> reinforcing and rewarding effects
alcohol and opioid peptide system
activates it
reinforcing and rewarding effects (mu)
craving
alcohol acutelystimulating gaba system causes what
sedative and anxiolytic effects
w drawal
alcohol inhibiting glutamate system causes
neuroadaptation and w drawal
alcohol results in an increase/decrease of DA release in the nucleus accumbens
inc
ethanol pk
lipid sol
non ppb
2 carbon moiety
1st order abs!!
metabolism is ) order (mikhaelis menten, capacity limited/fixed amt drug metab per unit time)
VERY low kM (conc where 50% of metabolism is saturated)
vMax (max amt cleared per hr) unrelated to how much drank
ethanol pk
begins w in 5 min of ingestion
lipids and proteins delay abs
75% abs in small int, 25% stomach
rapid gastric emptying and alcohol graphs
inc rate of gastric emptying–> more to small int–. more abs–> inc peak conc, inc curve sharpness, inc AUC
6 things that slow abs rate
- food in stomach
- carbs and amino acids
- cigarettes
- anticholinergics propantheline (delay gastric emptying)
- trauma, shock, massive blood loss
6 things that inc rate of absorption
- drinking in am after overnight fast
- drinks w higher % etOH
- carbonated drinkfs
- metoclopramide, erythromycin, cisapride (inc gastric emptying)
- low BG
- gut surgery (gastric bypass, gastrectomy)
rank Vd of alcohol, and why
male female obese
obese–> female–> male (highest)
alcohol distributes into TBW and lean, not fat. obese patients have dec TBW, females have more fat than males and a lower Vd compared to a male
who would get the highest BAC on the same beverage, all weigh 160lb
1. obese male who has not eaten all day
2. male who works out regularly and had light lunch
3. male drinking in the morning after no breakfast and going to the gym like he does 5x/week
1
male vs female alcohol dehydrogenase
women have less efficient pre-hepatic alcohol dehydrogenase –> greater bioavailability
inc Vd _______ BAC
(inc fat –> dec TBW) dec Vd –> inc BAC
CNS and chronic AUD effects
addiction
wernicke-korsakoff syndrome (wernicke’s encephalopathy)
cortical atrophy/dementia
hepatic and pancreatic effects of AUD chronic
steatosis, fatty liver
alcohol hepatitis
cirrhosis
pancreatitis
wernickes encephalopathy s/sx and patho
d/t acute deficiency in thiamine
sx: confusion, ataxia, leg tremor, visoin changes, nystigmus, dyplopia, eyelid drooping
wernickes encephalopathy pt in ER and MD wants to give D5W, is this ok?
NO! per krebs, thiamine is needed first to allow utilization of glucose
wernicke-korsakoff syndrome
patho
s/sx
results from long-standing wernickes
antegrade amnesia
memory loss
confabulation
hallucinations
FAS (fetal alcohol syndrome)
s/sx
small head, face deformities, hands and feet too
heart liver and renal defects
vision and hearing problems
CNS issues and developmental delays
short attention span
hyperactivity, anxiety, social w drawal
tolerance is due to
GABA receptor downregulation
in withdrawal …
GABA activation is low, NMDA is high and neurons are hyperexcitable
minor withdrawal timing and sx
5-10 hours
autonomic hyperactivity, tremors, hyperhydrosis, tachy c, HTN, GI upset, anxiety, insomnia, vivid dreams
major withdrawal timing and sx
12-72 hours
hallucinations (sensory bugs on skin), seizures generalized tonic-clonic
delirium tremens timing and sx
48-96 hours
in 5% of pts who w drawal
lasts 1-5 days
visual and auditory hallucinations
disordered consciousness
low grade fever
agitation
diaphoresis
disorientation
hypervent and resp alkalosis
sensorium clouding
life-threatening state - medical emergency!!
ethanol vs heroine withdrawal
higher risk of seizures, metabolic crisis, CV risks
w/drawal seizures
timing
s/sx
within 48 hours of last drink
generalized tonic-clonic
3% who seize develop status epilepticus
Delirium tremens mortality risk is greater in the
elderly
concominant COPD
core body temp >104
death usually dt arrhythmia or secondary complications (pneumonia, liver failure)
management / prophylaxis of alcohol withdrawal
4 things
thiamine 50 - 100mg daily
D5 and 1/2 NS
multivitamin
standing orders clonidine, benzos
CIWA score
definition
scale
measures sx of wd
<8-10: monitor q4-8h, non-pharm supportive care
8-15: benefit from pharm tx to redice complicaiton risk
>15: high risk for severe complications if no tx
benzos in alcohol w drawal
med, dose, freq, CIWA score correlation,
see note sheet
sobriety maintenance
group support
disulfram, naltrexone, acamprostate
drugs that can ppt disulfram rxn
nitromidazoles (metronidazole)
1st gen SUs (tolbutamine)
cephalosporins (cefoperazone, cefotetan)
griseofluvin
disulfram moa
dose
inhibits aldehyde dehydrogenase so acetylaldehyde builds up
do not admin until abstained for 12+ hrs
50mg qd x1-2 weeks initial
maintenance: 250mg qd
disulfram AE
CNS: drowsy, HA, fatigue
rash, allergic dermatitis
GI: metallic or garlic taste
hepatitis
peripheral neuropathy, neuritis
ocular neuritis
disulfram-disease concerns
diabetes, hepatic impairment, hypothyroidism, nephritis, seizures!!
naltrexone
dose
50mg qd
IM 380mg q4wk
acamprostate
moa
dose
structurally similar to GABA R’s, enhances GABA activity, dec glutamate activity
666mg po TID
