Benzodiazepines and Barbiturates Toxicology

A set of question-and-answer flashcards covering key mechanisms, clinical features, diagnosis, and management of benzodiazepine and barbiturate toxicity.

What therapeutic effects make benzodiazepines widely prescribed?

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

Why are benzodiazepines among the most frequently misused drugs?

Their widespread availability and desirable CNS effects lead to frequent misuse, overdose, and toxicity.

Through which neurotransmitter mechanism do benzodiazepines exert their primary effects?

They potentiate the activity of γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the CNS.

List three physiologic roles of GABA relevant to benzodiazepine action.

Sleep induction, control of neuronal excitation/epileptic potentials, and modulation of anxiety and memory.

Why are deaths from isolated benzodiazepine overdose rare?

Benzodiazepines have a high therapeutic index, especially when taken alone and managed appropriately.

What clinical feature is the hallmark of benzodiazepine overdose?

CNS depression leading to drowsiness, stupor, ataxia, or low-grade coma without major cardiorespiratory compromise.

How do most benzodiazepine-overdosed patients respond to stimulation?

They can usually be aroused with verbal or painful stimuli.

Which patient population often experiences prolonged coma after benzodiazepine overdose?

Elderly patients.

Name three common recovery-phase symptoms after benzodiazepine overdose.

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

What combination of drugs dramatically increases the risk of fatal respiratory depression in overdose?

Benzodiazepines combined with barbiturates (synergistic effect).

Which screening test is most useful for rapid identification of benzodiazepines in unknown CNS depression?

Qualitative urine immunoassay for parent benzodiazepines or their metabolites.

What confirmatory laboratory methods follow a positive benzodiazepine screen?

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

Give four drug classes that must be differentiated from benzodiazepine toxicity due to similar CNS depression.

Alcohols, barbiturates, opiates, antipsychotics (plus antiepileptics, muscle relaxants, CO, etc.).

What is the cornerstone of treatment for benzodiazepine overdose?

Supportive care: airway protection, assisted ventilation if needed, and cardiovascular support.

List three initial monitoring or treatment steps for significant benzodiazepine overdose.

Continuous cardiac monitoring, IV access, ECG (plus O2, pulse oximetry, thiamine, dextrose, naloxone as indicated).

How should a semi-comatose benzodiazepine patient be positioned to reduce aspiration risk?

Left lateral, head-down position.

When is single-dose activated charcoal most beneficial after benzodiazepine ingestion?

If administered within 1 hour of ingestion.

What is the specific benzodiazepine antagonist and its major limitation?

Flumazenil; it has a short half-life (~57 min) causing possible re-sedation 1–2 h later.

After how many hours of observation are most isolated benzodiazepine overdoses medically safe for discharge?

4–6 hours, provided they ambulate safely and psychiatric evaluation is completed.

For what clinical reasons should a benzodiazepine overdose patient be admitted after 6 h?

Persistent CNS depression or continued evidence of mild toxicity.

List three primary clinical uses of barbiturates.

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

Describe the mechanism by which barbiturates depress neuronal activity.

They enhance GABA-mediated chloride currents via a barbiturate receptor, causing synaptic inhibition.

What two factors cause hypotension with large barbiturate doses?

Depression of central sympathetic tone and direct depression of cardiac contractility.

Which respiratory effect occurs at high barbiturate doses?

Depression of medullary respiratory centers inhibiting all respiratory drives.

What symptoms characterize mild-to-moderate barbiturate intoxication?

Lethargy, slurred speech, nystagmus, and ataxia.

Why are clinical signs more reliable than plasma phenobarbital levels in assessing toxicity severity?

Because severity correlates better with CNS depression signs than with measured concentrations.

What are the fundamental components of emergency care in barbiturate overdose?

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

How does urine alkalinisation aid phenobarbital elimination, and what limitation exists?

Alkalinising urine to pH 7.5–8 increases clearance of long-acting barbiturates (e.g., phenobarbital); it is ineffective for short/intermediate-acting barbiturates and may cause fluid overload.

When is haemodialysis indicated for barbiturate poisoning?

In renal/cardiac failure, electrolyte or acid-base disturbances, or severe overdose, especially with long-acting barbiturates.