Benzodiazepines and Barbiturates Toxicology Review

A comprehensive set of question-and-answer flashcards covering 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 actions.

All benzodiazepines are clinically effective for treating which two common conditions?

Anxiety and insomnia.

Why are benzodiazepines among the most frequently misused drugs?

Their widespread availability and desirable CNS-depressant effects increase misuse potential.

How does the dependence and abuse liability of benzodiazepines compare with alcohol, cocaine, or opiates?

It is generally lower than that of alcohol, cocaine, or opiates.

By what mechanism do benzodiazepines exert their CNS effects?

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

List three physiologic processes in which GABA is involved.

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

What is the hallmark clinical feature of benzodiazepine overdose?

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

Can most benzodiazepine-overdosed patients be aroused with stimulation?

Yes; verbal or painful stimuli usually arouse them unless co-ingestants are present.

Which patient population may experience prolonged coma after benzodiazepine overdose?

Elderly patients.

Name three common post-recovery symptoms following benzodiazepine overdose.

Dizziness, depression, and apathy.

Profound coma or respiratory failure after oral benzodiazepine overdose is most likely when what circumstance exists?

Co-ingestion with other depressants (e.g., barbiturates) or intravenous administration.

Why is the benzodiazepine-barbiturate combination considered dangerous?

Synergistic CNS depression causes ~50 % of such patients to need mechanical ventilation.

What initial laboratory test quickly aids diagnosis of unexplained CNS depression possibly due to benzodiazepines?

Qualitative urine immunoassay screening for benzodiazepines or their metabolites.

Which confirmatory techniques verify a positive urine benzodiazepine screen?

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

Give four toxicologic or medical conditions that can mimic benzodiazepine toxicity.

Alcohol intoxication, opiate overdose, carbon-monoxide poisoning, head trauma (also antipsychotic overdose, metabolic disturbances, etc.).

What are the first priorities in managing significant benzodiazepine overdose?

Protect airway, assist breathing, provide cardiovascular support (ABCs).

List three routine monitoring interventions for benzodiazepine-overdose patients.

Continuous cardiac monitoring, supplemental oxygen with pulse oximetry, and electrocardiography.

What single-dose gastrointestinal decontamination is preferred after recent benzodiazepine ingestion?

Activated charcoal 1 g/kg orally or via NG tube within 1 hour.

Name the specific benzodiazepine antagonist and state its mean half-life.

Flumazenil; mean half-life ≈ 57 minutes.

Why must patients receiving flumazenil be observed for at least 2 hours?

Resedation can occur as the antagonist wears off.

After isolated benzodiazepine overdose, how long is emergency-department observation usually sufficient?

4–6 hours if only minimal to mild toxicity develops.

When should a benzodiazepine-overdose patient be admitted to a monitored bed?

If significant CNS depression persists or any toxicity remains at 6 hours.

State three primary clinical uses of barbiturates.

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

Describe the basic mechanism of barbiturate-induced CNS depression.

They enhance GABA-mediated chloride currents via the barbiturate receptor, leading to neuronal inhibition.

What two mechanisms cause hypotension after large barbiturate doses?

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

How do barbiturates depress respiration at high doses?

They inhibit medullary respiratory centers, blocking all three respiratory drives.

List four early signs of mild to moderate barbiturate intoxication.

Lethargy, slurred speech, nystagmus, and ataxia.

What pupil size and reflex status are typical in deep barbiturate coma?

Small or mid-position pupils with loss of reflex activity (patient may appear dead).

Why is hypothermia common in severe barbiturate poisoning?

Deep coma plus environmental exposure decreases heat production and promotes heat loss.

Which laboratory value is especially helpful in suspected phenobarbital overdose?

Serum phenobarbital concentration.

What is the cornerstone of emergency treatment for barbiturate poisoning?

Supportive care: airway protection, ventilation, oxygen, IV access, treatment of hypotension and hypothermia.

Is there a specific antidote for barbiturate overdose?

No; management is supportive, as no specific antagonist exists.

How can gastrointestinal decontamination be achieved after barbiturate ingestion?

Prompt activated charcoal; gastric lavage or emesis if within 24 h and large ingestion.

Why might urinary alkalinisation be attempted in phenobarbital overdose, and what are its limitations?

Alkaline urine (pH 7.5–8) increases clearance of long-acting barbiturates like phenobarbital; it is ineffective for short/intermediate barbiturates and risks fluid overload.

When is haemodialysis recommended in barbiturate toxicity, and for which type is it most effective?

If renal/cardiac failure or major acid–base/electrolyte issues arise; more effective for long-acting barbiturates due to lower protein/lipid binding.