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Can you name the Alcohols?

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Drug P-kinetics: Zero order kinetics (saturatable). Ethanol converted to acetaldehyde by alcohol dehydrogenase (NAD+ required). Acetaldehyde converted to acetate by aldehyde dehydr
Clinical Use: Reduce seizure threshold and stop seizure activity during ethanol withdrawal
Drug SE: Toxicities are why it is used. Inhibits metabolism of other drugs. Hepatotoxicity
Drug MOA: Inhibits alcohol dehydrogenase
Drug MOA: Required for synthesis of the coenzyme thiamine pyrophosphate
Fomepizole class
Drug SE: Hepatotoxicity, avoid w/ disulfiram. Precipitate withdrawal in patients using heroine or other opioids.
Methanol class
Drug P-kinetics: IV, oral short acting, no active metabolites,
Drug SE: Allergies, tachycardia, BP changes, flatulence, impotence, GI distress & rash
Drug Tx: Ethanol IV w/ dextrose in water or Fomepizole to inhibit conversion by alcohol dehydrogenase. Hemodialysis. Bicarbonate for acidosis. Folic acid to speed breakdown of form
Drug P-kinetics: Alcohol dehydrogenase converts ethylene glycol into oxalic acid (renal toxic crystals)
Disulfiram class
Drug to decrease chronic ethanol use
Chronic toxicity: liver dz, CA, accidents, suicide, chronic pancreatitis, gastritis, malabsorption of vitamins. Tolerance & dependence, Neurotoxicity (Wernicke-Korsakoff syndrome),
Drug Use: Deterrent to relapse in individuals w/ alcoholism. After one drink acetaldehyde accumulates producing unwanted side effects of HA, flushing, n/v, & hypotension
Oxazepam class
Drug SE: Visual disturbances ('snow storm'), blurred vision, retinal damage. Formaldehyde on breath or urine, bradycardia, prolonged coma, seizures, severe metabolic acidosis w/ el
Drug SE: Seizures, HA, nausea, dizziness, rash, metallic taste, abnormal smell, rare allergic reactions.
Drug MOA and tox: metabolized by alcohol dehydrogenase to oxalic acid.
Drug MOA & tox: Formaldehyde formed by conversion of methanol via alcohol dehydrogenase results in in toxicity
Drug P-kinetics: IV until asymptomatic
Drugs use: Reduce cravings for alcohol & alcohol relapse (when given with counseling) in the short term. Reduces subjective 'high' assoc w/ alcohol.
Drug Acute Mgmt: Prevent respiratory depression & aspiration, glucose to manage hypoglycemia & thiamine to protect against Wernicke-Korsakoff syndrome
Drug P-kinetics: Oral delayed release
Drug P-kinetics: IV
Drug MOA: Inhibits aldehyde dehydrogenase producing accumulation of acetaldehyde after the consumption of alcohol
Drug use: Prevent the conversion of either ethylene glycol or methanol by alcohol dehydrogenase into toxic compounds (oxalic acid or formaldehyde, respectively).
Drug MOA: Competitive NMDA receptor antagonist?
Drug P-kinetics: Oral short acting, no active metabolites,
Naltrexone class
Drug MOA: Opioid receptor antagonist. Mu opioid antagonist--decreases opioid binding in reward pathways
Clinical Use: Used for methanol, ethylene glycol poisoning. Given IV (5-10% w/ 5% dextrose in H2O) to saturate alcohol dehydrogenase
Diazepam class
Drug Tx: Key to dx is anion gap acidosis, osmolar gap, & oxalate crystals in urine. Tx: similar to methanol poisoning. 4-methylpyrazole (an inhibitor of alchohol dehydrogenase) if
Acute toxicity: dose dependent CNS depressant, CV depressant, smooth muscle relaxant.
Drug P-kinetics: Metabolized by alcohol dehydrogenase to formaldehyde. Formaldehyde is metabolized to CO2 by folate-dependent systems
Drug SE: none
Drug SE: Stages - 1) Acute Stage (minutes): excitation followed by CNS depression. 2) 4-12 hrs = severe metabolic acidosis (acid metabolites accumulate), anion gap & osmolar gap ac
Drug Use: To prevent Wernicke-Korsakoff syndrome in chronic alcoholics
Drug MOA: Increase frequency of firing of GABA-A chloride channels
Lorazepam class
Drug P-kinetics: IM injections (monthly) or oral (Daily)
Drug Withdrawal Mgmt: Withdrawal symptoms (motor agitation, anxiety, insomnia, seizures, visual hallucinations, delirium tremens): Mild--thiamine, restore electrolytes. Moderate to
Thiamine class (B1)
Acamprosate class
Drug MOA: Alters membrane-bound neuronal ion conductance & GPCR receptors: Acute decrease NMDA channel conductance & increase GABA-A Cl- channel conductance. Chronic exposure: adap
Drug P-kinetics: IV, long acting--self tapering
Ethylene glycol class
Ethanol class
Drug P-kinetics: Oral

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