Flashcards in Alcohol Deck (23)
BAC intoxication level in most states
Name the BAC level:
-Sedation, subjective “high,” slower reaction times
-Impaired motor function, slurred speech, ataxia
-Respiratory depression, death
50-100 - Sedation, subjective “high,” slower reaction times
100-200 - Impaired motor function, slurred speech, ataxia
200-300 - Emesis, stupor
300-400 - Coma
>500 - Respiratory depression, death
The two CNS ion channels that ethanol targets.
- NMDA subtype of glutamate receptors
What are NMDA and GABA receptor functions in the CNS?
NMDA is the primary EXCITATORY NT.
GABA is the primary INHIBITORY NT .
Alcohol inhibition of NDMA and GABA results in loss of what normal functions of each?
NMDA - normally implicated in learning/memory. Alcohol inhibits the ability of glutamate to open the cation channel of the NMDA receptor and leads to a depression of the CNS.
GABA is normally implicated in depression of CNS. Alcohol enhances GABA effects.
Tolerance and dependence have opposite effects on NMDA and GABA than alcohol (making you drink more to get same effect).
Symptoms of ____ include:
-hyperexcitability/palpitations, **tremors, anxiety, insomnia,** N/V, in mild cases
-seizures, toxic psychosis, and delirium tremens in severe cases
What is characterized by delirium, hallucinations, fever, and tachycardia? How long after alcohol discontinuation does this begin?
Associated with thiamine deficiency, symptoms show: Paralysis of the external eye muscles, ataxia, and a confused state that can progress to coma and death.
Treatment of this
Thiamine to improve ocular problems, ataxia, confusion.
Peripheral nerve injury, gait and ataxia, dementia, painless blurring vision. all indicate?
Neurotoxicity from alcohol
Ethanol increases levels of ___ enzyme, leading to what drug-drug interaction?
CYP450, leading to acetaminophen-induced hepatotoxicity
Drugs for treatment of acute alcohol withdrawl
diazepam (long acting benzos), lorazepam and oxazepam (short acting benzos, good for people with iver dz), and thiamine
Drugs for prevention of alcohol abuse/dependence
acamprosate, disulfram, naltrexone
Drugs for treatment of acute methanol or ethylene glycol poisoning
ethanol and fomepizole
Management of acute alcohol intoxication
glucose, thiamine, potassium (if severe vomiting)
MOA of___: µ opioid receptor antagonist (long-acting). reduces craving for alcohol. Used to reduce cravings and relapse. For tx of alcohol and opiate dependence.
Contraindicated in patients with what two conditions
CI in hepatitis and liver failure
MOA of ___: weak NMDA-receptor antagonist and GABAA receptor agonist (also affects serotonergic, noradrenergic, and dopaminergic systems). Used to reduce relapse (long+short term).
Contraindicated in what disease?
CI in renal disease
MOA of ___: irreversibly inhibits aldehyde dehydrogenase and causes extreme discomfort in
patients who drink alcoholic beverages (flushing, throbbing headache, nausea, vomiting, sweating, hypotension, confusion due to the accumulation of aldehyde).
Four part treatment of ___ poisoning - when a person comes in with blurred vision "like being in a snowstorm".
(1) Respiratory support
(2) Suppression of metabolism by ADH (**ethanol and fomepizole**)
(3) Hemodialysis to enhance methanol removal
(4) Alkalinization to counteract metabolic acidosis (bicarbonate)
**ETHANOL has a higher affinity than methanol for ADH and is often.**
Fomepizole inhibits ADH and also used for tx.
A pet/child ingests antifreeze or an industrial solvent with ethylne glycol. Treatment?
Hemodialysis, ethanol infusion, fomepizole
Inhibits alcohol dehydrogenase.
Inhibits aldehyde dehydrogenase
Ethanol undergoes extensive first-pass metabolism by gastric and liver ___
alcohol dehydrogenase (ADH)