| Hint | Answer |
|---|
| Drug Use: To prevent Wernicke-Korsakoff syndrome in chronic alcoholics | |
| 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 | |
| Drugs use: Reduce cravings for alcohol & alcohol relapse (when given with counseling) in the short term. Reduces subjective 'high' assoc w/ alcohol. | |
| Clinical Use: Reduce seizure threshold and stop seizure activity during ethanol withdrawal | |
| 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 | |
| Lorazepam class | |
| Drug P-kinetics: Zero order kinetics (saturatable). Ethanol converted to acetaldehyde by alcohol dehydrogenase (NAD+ required). Acetaldehyde converted to acetate by aldehyde dehydr | |
| 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 MOA: Competitive NMDA receptor antagonist? | |
| Drug SE: Seizures, HA, nausea, dizziness, rash, metallic taste, abnormal smell, rare allergic reactions. | |
| Drug SE: Toxicities are why it is used. Inhibits metabolism of other drugs. Hepatotoxicity | |
| Chronic toxicity: liver dz, CA, accidents, suicide, chronic pancreatitis, gastritis, malabsorption of vitamins. Tolerance & dependence, Neurotoxicity (Wernicke-Korsakoff syndrome), | |
| Thiamine class (B1) | |
| Ethanol class | |
| 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 | |
| Acute toxicity: dose dependent CNS depressant, CV depressant, smooth muscle relaxant. | |
| Drug P-kinetics: Oral short acting, no active metabolites, | |
| Drug use: Prevent the conversion of either ethylene glycol or methanol by alcohol dehydrogenase into toxic compounds (oxalic acid or formaldehyde, respectively). | |
| Methanol class | |
| Drug SE: Hepatotoxicity, avoid w/ disulfiram. Precipitate withdrawal in patients using heroine or other opioids. | |
| Drug Withdrawal Mgmt: Withdrawal symptoms (motor agitation, anxiety, insomnia, seizures, visual hallucinations, delirium tremens): Mild--thiamine, restore electrolytes. Moderate to | |
| Drug MOA: Inhibits aldehyde dehydrogenase producing accumulation of acetaldehyde after the consumption of alcohol | |
| Drug P-kinetics: IM injections (monthly) or oral (Daily) | |
| Disulfiram class | |
| Drug P-kinetics: Oral | |
| | Hint | Answer |
|---|
| Drug P-kinetics: Alcohol dehydrogenase converts ethylene glycol into oxalic acid (renal toxic crystals) | |
| Drug P-kinetics: IV until asymptomatic | |
| Drug MOA & tox: Formaldehyde formed by conversion of methanol via alcohol dehydrogenase results in in toxicity | |
| Drug MOA: Increase frequency of firing of GABA-A chloride channels | |
| Drug P-kinetics: IV | |
| Diazepam 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 P-kinetics: IV, oral short acting, no active metabolites, | |
| Drug P-kinetics: Metabolized by alcohol dehydrogenase to formaldehyde. Formaldehyde is metabolized to CO2 by folate-dependent systems | |
| Drug to decrease chronic ethanol use | |
| Drug Acute Mgmt: Prevent respiratory depression & aspiration, glucose to manage hypoglycemia & thiamine to protect against Wernicke-Korsakoff syndrome | |
| Drug MOA: Required for synthesis of the coenzyme thiamine pyrophosphate | |
| Drug P-kinetics: IV, long acting--self tapering | |
| Ethylene glycol class | |
| Drug P-kinetics: Oral delayed release | |
| Acamprosate class | |
| Oxazepam class | |
| Drug SE: none | |
| Fomepizole class | |
| Drug SE: Allergies, tachycardia, BP changes, flatulence, impotence, GI distress & rash | |
| Drug MOA: Inhibits alcohol dehydrogenase | |
| Naltrexone class | |
| Drug MOA and tox: metabolized by alcohol dehydrogenase to oxalic acid. | |
| Drug Use: Deterrent to relapse in individuals w/ alcoholism. After one drink acetaldehyde accumulates producing unwanted side effects of HA, flushing, n/v, & hypotension | |
| 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 | |
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