Benzodiazepines & Barbiturates – Toxicology and Management

Question-and-answer flashcards reviewing pharmacology, toxicity, diagnosis, and management of benzodiazepine and barbiturate overdose.

What therapeutic effects make benzodiazepines widely prescribed?

Sedative, hypnotic, amnestic, anxiolytic, anticonvulsant, and muscle-relaxant actions.

All benzodiazepines are effective in treating which two common disorders?

Anxiety and insomnia.

Compared with alcohol, cocaine, or opiates, how significant is benzodiazepine dependence and abuse?

Generally minor, though misuse is still frequent due to wide availability.

Through what primary mechanism do benzodiazepines exert their CNS effects?

Potentiation of γ-aminobutyric acid (GABA) activity at the GABA_A receptor.

Name three physiological roles of GABA relevant to benzodiazepine action.

Sleep induction, control of neuronal excitation/epileptic potentials, and anxiety modulation (also memory and HPA axis regulation).

Why are fatal outcomes rare in isolated benzodiazepine overdose?

They possess a high therapeutic index; serious cardiopulmonary compromise is uncommon when taken alone.

What clinical hallmark signifies benzodiazepine overdose?

CNS depression leading to drowsiness, stupor, ataxia, or low-grade coma.

How can most patients in benzodiazepine coma be aroused?

With verbal or painful stimulation.

Which patient group often experiences prolonged coma after benzodiazepine overdose?

Elderly patients.

List three benign recovery symptoms after benzodiazepine overdose that usually require only supportive care.

Dizziness, depression, and apathy (with possible mild hypothermia, bradycardia, hypotension).

Why is the combination of benzodiazepines and barbiturates dangerous?

Synergistic CNS/respiratory depression—about 50 % of such cases need mechanical ventilation and may be fatal.

What initial laboratory test quickly detects benzodiazepines in unknown CNS depression?

Qualitative urine immunoassay screen for parent drug or metabolites.

How are positive benzodiazepine screens confirmed?

Gas or high-pressure liquid chromatography and/or mass spectrometry.

Give three toxicologic or medical conditions that mimic benzodiazepine overdose.

Alcohol intoxication, opiate overdose, carbon monoxide poisoning (also antipsychotics, barbiturates, head injury, CVA, etc.).

Primary management priorities in significant benzodiazepine overdose?

Airway protection, assisted breathing, cardiovascular support (ABC).

What routine monitoring is recommended for benzodiazepine-overdose patients?

Continuous cardiac monitor, IV access, ECG, pulse oximetry, vital-sign and neurologic checks.

Why are thiamine, dextrose, and naloxone sometimes given empirically in altered mental-status cases?

To treat or rule out hypoglycemia, Wernicke’s encephalopathy, or opioid co-ingestion.

Optimal patient position to reduce aspiration risk in semi-comatose benzodiazepine overdose?

Left lateral, head-down (recovery) position.

When is activated charcoal most beneficial after benzodiazepine ingestion?

Within 1 hour of ingestion at 1 g/kg orally or via NG tube.

Name the benzodiazepine antidote and its major limitation.

Flumazenil; short half-life (~57 min) causing potential resedation and need for repeat dosing.

Typical emergency-department observation period before discharge after isolated benzodiazepine overdose?

4–6 hours if toxicity remains mild and patient can ambulate safely.

List three medical uses of barbiturates.

Hypnotic/sedative agent, induction of anaesthesia, treatment of epilepsy/status epilepticus.

Describe the primary mechanism of barbiturate toxicity.

Generalized neuronal depression via enhanced GABA-mediated chloride currents and postsynaptic inhibition.

What causes hypotension in large barbiturate overdoses?

Depressed central sympathetic tone plus direct myocardial contractility depression.

At very high doses, how do barbiturates affect respiration?

Depress medullary respiratory centers, inhibiting all three respiratory drives and risking apnea.

Key clinical signs of mild-moderate barbiturate intoxication?

Lethargy, slurred speech, nystagmus, and ataxia.

Which complications are common in deep barbiturate coma?

Hypothermia, hypotension, bradycardia, small/mid-position pupils, loss of reflexes.

Why are clinical signs preferred over serum levels for assessing barbiturate toxicity severity?

Signs and symptoms correlate more reliably with clinical outcome than plasma concentrations.

First-line supportive measures in barbiturate overdose management?

Airway protection, 100 % oxygen, IV access, treat coma ("coma cocktail"), manage hypothermia and hypotension.

Which elimination technique specifically increases phenobarbital clearance and when is it recommended?

Urine alkalinisation to pH 7.5–8.0 for long-acting barbiturates; benefit uncertain and may cause fluid overload.

When is hemodialysis indicated in barbiturate poisoning?

Renal/cardiac failure, severe electrolyte or acid-base disturbances; more effective for long-acting barbiturates.