Alcohol Use and Abuse (PHARM) Flashcards
administration of ___ will prevent the metabolism of methanol or ethylene glycol
ethanol (compettive inhibitor) or fromepizole
MOA Fomepizole
inhibits alcohol dehydrogenase
MOS Disulfiram
inhibits adehyde dehydrogenase
**used to encourage abstinence from alcohol bc it allows for the accumulation of intermediate (acetaldehyde) which leads to nausea and flushing
difference in metabolism in chronic alcoholic
chronic alcohol use induces CYP actions
why do some alcoholics find acetaldyhyde pleasureable (and therefore like disulfram)
promotes DA release and condenses with DA to form salsolinol (an agent that reinfoces behavior (i.e. drinking)
why does alcohol and acetaminophen not mix
ethanol induces CYP which metabolizes acetaminophen to hepatotoxic intermediated NAPQI (which accumulates bc the reaction to convert NAPQI becomes depleted)
MOA of N-acetyl cysyeine
provides fresh conjugate substrate for NAPQI to be detoxified
Effect of ethanol on GABA
inc its release and receptor density
effect of ethanol on NMDA
inhibit post synaptic receptors
effect of ethanol on DA
increase release and effected in VTA
effects of ethanol on ATCH
inc levels of it in the blood
effects of ethanol on opiod
release of Beta endorphins and activation of mu receptors
effects of ethanol on 5-HT
inc 5-HT in synaptic space
more fat content correlate to higher or lower BAL
higher bc ethanol does not distribute to adipose
effects of chronic alcoholism on the liver
dec gluconeogenesis--> hypoglycemia fatty liver (hepatitis and chirrosis)
effects of chronic alcoholism on the GI tract
bleeding ans scaring –> abs an nutritional def
effects of chronic alcoholism on the CNS
peripheral neuropathy
Werike-Kosakoff syndrome = ataxia, confusion, ocular muscle paralysis
effects of chronic alcoholism on endocrine sys
dec steroid production –> gynocomastia and testicular atrophyy
Fetal Alcohol Syndrome is characterized by
IU growth retardation Microcephaly Poor coordination flattened face (midfacial underdevelopment) minor joint abnormalities
treatment for intoxicated pt vs withdrawing pt (from alcohol)
intox: thamine then D50 then correct electrolytes
withdrawal: BNZ sedative (diazepam or laorazepam if hepatic function compromised (has shorter t1/2 due to metabolism by glucuronidation))
drugs that have disulfram effects
sufonylureas, ceftotetan, ketoconazole, and procarbazine
MOA and effect of Naltrexone
mu opioid antagonist to de the feelings of reward or cravings
MOA and effect if Acamprostate
activator of GABA receptors and weak NMDA antagonist
dec reinforcement/reward
How is NAPQI detoxified
conjugated to cysteine or mercapturic acid
what BAL is needed to cause coma, resp insuff, and death
> 400 mg/dL
What BAL is needed to cause limited muscle in coordination? pronounced incoordination? ataxia?
< 50
50-100
150-400
at what BAL will you see mood and personality changes
100-150
what is the mech behind blackouts?
NMDA/glutamate receptor inhbibition by the ethanol
why is thiamine given before D50?
if not can exacerbate wernikie-korsakoff syndrome
What areas of the brain are activated to reinforce alcohol addiction via activation of reward
VTA and nucleus accumbans
competitive alcohol dehydrogenase inhibitor
fromepizole (prevent met of alcohols)
