NSG 211: Addiction Pharmacology

Comprehensive practice flashcards covering addiction pharmacology including alcohol detoxification and relapse prevention, benzodiazepine/barbiturate tapering, supportive micronutrient therapy, and opioid use disorder management from NSG 211 lecture notes.

What is the first-line medication class used to treat acute alcohol withdrawal?

Benzodiazepines (such as chlordiazepoxide, diazepam, and lorazepam) are first line because they bind GABA receptors, replace alcohol via cross-tolerance, and prevent withdrawal seizures and delirium tremens (DTs).

Why must thiamine (vitamin B1) be given to every patient undergoing alcohol detoxification?

Alcohol impairs B-vitamin absorption and patients often have poor intake; thiamine replacement is essential to prevent Wernicke encephalopathy and its progression to irreversible Korsakoff syndrome.

Why is frequent monitoring and repeat dosing necessary when administering naloxone (Narcan) for opioid overdose?

Naloxone has a shorter half-life than many opioids, meaning the opioid can outlast the antagonist and cause recurrent central nervous system and respiratory depression (re-sedation).

How long must a patient be opioid-free before beginning naltrexone (ReVia, Vivitrol), and why?

Patients must be opioid-free for $7\text{--}10$ days ($6\text{--}10$ days per K&S, or at least $1$ week per Lilley) to prevent the precipitation of acute, severe opioid withdrawal.

What alcohol exposure precautions must a patient follow while taking disulfiram (Antabuse)?

The patient must maintain zero alcohol intake in any form—including hidden sources such as cough syrups, mouthwashes, aftershaves ("skin bracers"), and colognes—and avoid alcohol for $3\text{--}4$ days after stopping the medication.

How does chlordiazepoxide (Librium) work to manage alcohol withdrawal?

It binds to GABA-benzodiazepine receptors, mimicking alcohol through cross-tolerance, thereby substituting for alcohol and calming rebound central nervous system excitation.

Can autonomic adjuncts such as clonidine or beta-blockers replace benzodiazepines in alcohol withdrawal?

No. Adjuncts can help control tachycardia and hypertension, but they never replace benzodiazepines for preventing withdrawal seizures and delirium tremens (DTs).

What is the typical dosing timeline and pattern for chlordiazepoxide during alcohol withdrawal?

Dosing is guided by the CIWA-Ar scale using oral tapering doses; withdrawal symptoms peak around $24\text{--}48\,\text{h}$, and the taper is stopped after day $5$.

What are the primary clinical indications for diazepam (Valium) in addiction medicine?

First-line management of alcohol withdrawal, benzodiazepine withdrawal tapers, and treatment of seizures and agitation associated with stimulant (e.g., cocaine) intoxication.

What is the dosing schedule for a benzodiazepine withdrawal taper using diazepam per Lilley?

$10\text{--}20\,\text{mg}$ PO four times daily on day $1$, tapered down to $5\text{--}10\,\text{mg}$ on the last day over $7\text{--}10$ days ($10\text{--}14$ days for long-acting agents), avoiding PRN dosing.

What contraindications exist for the administration of diazepam?

Known drug allergy, airway obstruction or dyspnea, narrow-angle glaucoma, and porphyria.

What clinical pearl highlights the safety profile of diazepam relative to concurrent alcohol ingestion?

Diazepam alone rarely kills; diazepam combined with alcohol can.

Why is lorazepam (Ativan) preferred over chlordiazepoxide or diazepam in patients with liver impairment?

Lorazepam is shorter-acting and simpler to clear via glucuronidation without extensive hepatic oxidation, summarized by the clinical pearl: "Liver is Lousy (\rightarrow) Lorazepam."

According to K&S Table 31.3, what are oxazepam (Serax) and hydroxyzine (Vistaril) used for in alcohol treatment?

Oxazepam (Serax) is used in tapering doses for alcohol withdrawal, and hydroxyzine (Vistaril) is used for sleep.

When does barbiturate withdrawal typically begin, and what severe complications can occur?

Withdrawal starts $8\text{--}12\,\text{h}$ after the last dose and can cause seizures and delirium.

How is a barbiturate withdrawal taper conducted according to Lilley?

Calculate barbiturate equivalence, administer $50\%$ of the original dose, and taper over $7\text{--}10$ or $10\text{--}14$ days ($2\text{--}4$ weeks per K&S) while avoiding PRN dosing.

What clinical signs should the nurse monitor for that suggest Wernicke-Korsakoff syndrome?

Confusion, ataxia, abnormal eye movements (nystagmus/ophthalmoplegia), confabulation, and peripheral neuropathy.

Why is acetaminophen used with caution in patients with a history of heavy alcohol consumption?

Chronic heavy alcohol intake induces CYP 2E1 enzymes, leading to increased production of toxic metabolites and severe liver damage even at standard doses.

What is the mechanism and role of clonidine (Catapres) in substance withdrawal?

An alpha-2 adrenergic agonist that relieves autonomic hyperactivity (sweating, anxiety, restlessness, elevated BP, diarrhea); it is the non-opioid choice for opioid withdrawal and an adjunct for alcohol withdrawal.

What symptoms of opioid withdrawal does clonidine NOT treat?

It does not treat opioid cravings or insomnia, nor does it prevent withdrawal seizures or delirium tremens.

What vital nursing assessment must be conducted prior to administering clonidine (Catapres)?

Check blood pressure before every dose, withhold if the patient is hypotensive, and educate the patient to rise slowly to prevent orthostatic hypotension.

What is the indication for IV propranolol in stimulant toxicity according to K&S?

It is administered intravenously to manage severe tachyarrhythmias resulting from cocaine intoxication.

How does naltrexone (ReVia, Vivitrol) aid in alcohol and opioid use disorders?

It blocks opioid receptors, reducing cravings and dampening the pleasure/reward sensation associated with drinking alcohol and using opioids.

What key distinction separates naltrexone from naloxone?

Naltrexone is a long-acting maintenance blocker for relapse prevention, whereas naloxone is a short-acting emergency antagonist used for immediate overdose reversal.

What critical educational point must patients taking naltrexone understand regarding analgesia?

Opioid pain medications will be completely blocked and ineffective; they must carry medical alert identification and maintain psychosocial counseling.

What is the primary rule for initiating acamprosate in alcohol use disorder?

The patient must already be abstinent ("Already at CAMP Sober") before starting acamprosate, as it maintains abstinence rather than inducing detox.

What is the proposed mechanism of action and clinical use of acamprosate?

It acts as a GABA agonist and glutamate antagonist to restore chemical balance in the brain, helping reduce post-withdrawal anxiety and protracted abstinence cravings.

What biochemical reaction occurs when a patient on disulfiram (Antabuse) ingests alcohol?

Disulfiram blocks aldehyde dehydrogenase, causing toxic acetaldehyde concentrations to increase $5\text{--}10\times$, precipitating acetaldehyde syndrome.

What are the common and severe manifestations of an acetaldehyde reaction from disulfiram?

Common: scarlet facial flushing, throbbing headache, copious vomiting, dyspnea, tachycardia, and hypotension within $5\text{--}10\,\text{min}$; Severe: arrhythmias, myocardial infarction, heart failure, seizures, coma, and death.

What is the minimum volume of alcohol capable of triggering a disulfiram reaction?

As little as $7\,\text{mL}$ of alcohol can trigger the reaction.

Which antimicrobial agent causes a disulfiram-like reaction when ingested with alcohol?

Metronidazole causes a disulfiram-like reaction when combined with alcohol.

What is nalmefene used for in addiction medicine according to Giddens?

It is an opioid antagonist used to reduce alcohol cravings during withdrawal and recovery.

What is the nurse's priority action when treating an opioid overdose alongside naloxone administration?

Ensuring airway, oxygenation, and ventilation first, while administering naloxone and obtaining emergency medical care.

Why does methadone (Dolophine) allow for once-daily dosing in opioid use disorder?

It possesses an extended elimination half-life ($15\text{--}30\,\text{h}$ per K&S; $12\text{--}24\,\text{h}$ per Lilley) compared to morphine ($\sim 2\,\text{h}$), suppressing drug hunger and withdrawal over a full day.

Why does methadone carry the greatest overdose risk among medications for opioid use disorder (MOUD)?

Because methadone is a full opioid agonist without a receptor ceiling effect, making it capable of causing severe respiratory depression and fatal overdose, particularly when combined with other CNS depressants.

What is the pharmacologic classification and receptor activity of buprenorphine (Subutex)?

It is a partial mu-opioid receptor agonist and kappa-opioid receptor antagonist.

What is the clinical advantage of buprenorphine's partial agonist mechanism compared to full agonists?

It demonstrates a "ceiling effect," meaning higher doses provide reduced withdrawal and craving relief with a lower risk of respiratory depression and fatal side effects.