Anxiolytics Flashcards

Synopsis This session introduces you to the neuropharmacological principles of anxiolytic, sedative and hypnotic therapeutics. The antidepressant drugs are covered more in-depth in the Yr2 LSRC Mood-Stabilising Therapeutics session. Learning Outcomes Describe* the mechanism of action, indications for use, relevant contraindications and adverse effects for the following drugs: *(to a depth to enable the anticipation of their clinical effects, communicate effectively with colleagues and counsel p (37 cards)

1
Q

Which anxiety symptoms are “physical/sympathetic” targets for beta-blockers?

A

A: Tremor, sweating, palpitations (somatic symptoms).

Anxiolytics, Sedatives Hypnoti…

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2
Q

Most common anxiety disorders

A

gad, agoraphobia, panic

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3
Q

Which neurotransmitter system do benzodiazepines and z-drugs enhance to reduce anxiety/sedate?

A

GABA-A inhibitory signalling.

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3
Q

Which is key structure in brain to regulating fear and anxiety
Studies show that people show heightened ______ response to anxirty

A

amygdala

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4
Q

Chemical imbalances: norepinephrine,serotonin,dopamineandgamma-aminobutyric acid (GABA).
Evidence for the role of brain-derived neurotrophic factor (BDNF) in modulating neural plasticity in anxiety states . i.e, down regulation of BDNF is found in anxiety states

A
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5
Q

why is there considerable overlap between anxiolytic sedative and hypnotic

Duh

A

Dose–response: increasing CNS inhibition → calming → sedation → sleep induction.

duh

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6
Q

Q: In GAD, where do benzodiazepines sit in stepped care?

A

A: Short-term option (not long-term first-line), while SSRIs !!!!! are the first-choice drugs in the same Step number 3

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7
Q

What receptor do benzodiazepines modulate, and what is its fast inhibitory ion?

A

GABA-A receptor; increases chloride (Cl⁻) conductance → neuronal inhibition.

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8
Q

Benzos are an agonist for GABA A what other things enhance its activity

A

Z drugs
Barbiturares
Alcohol

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9
Q

Benzodiazepines bind where on GABA-A and do what type of modulation
: What functional effect do benzodiazepines cause at the channel level?

A

A: Bind γ (gamma) subunit; positive allosteric modulation

benzos Increase frequency of channel opening → ↑ Cl⁻ influx → ↓ action potential firing.

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10
Q

Q: List the key clinical effects you must anticipate/counsel for benzodiazepines. important

A

A: Sedation, hypnosis (higher dose), anterograde amnesia, anxiolysis, anticonvulsant activity, reduced skeletal muscle tone.

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11
Q

SUPREMELY IMPORTANT
WHAT are the indcatons and time limits of benzodiazepine

A

Indicated for SHORT TERM RELIEF from SEVERE anxiety and INSOMNIA

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12
Q

what are z drugs? whats their indication

A

short term insomnia use

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13
Q

: Why choose a short-acting BDZ (e.g., temazepam) for insomnia, to act as a hypnotic (sleep inducing)

A

They are rapidly absorbed by the gut = fast sedation = short duration of morning ‘hangoer’ , -(by using drugs metabolized y inactive compounds)

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14
Q

why are the anxiolytic properties of beznodiazepines best used with a compound of a long duration

A

smaller dose is used for less sedation, long duration reduces rebound anxiety between doses seen w short acting doses

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15
Q

very important
Main adverse effect risk of long-term benzodiazepines?

Q: Who is at higher risk of benzodiazepine dependence/withdrawal problems?

A

Dependence with physical + psychological withdrawal.

Personality disorders; prior alcohol/drug dependence; high doses.

16
Q

common benzo wthdrawal symptoms?
Q: Severe withdrawal features (rare but serious)?

A

A: Anxiety (most common), insomnia, depression, perceptual sensitivity (noise/light/touch).
A - A: Psychosis or convulsions (rare)

17
Q

Q: How should long-term benzodiazepines be stopped?
What prescribing rule reduces dependence risk?

A

Q: How should long-term benzodiazepines be stopped?
A: Gradual withdrawal over ~4–8 weeks; sometimes full withdrawal can take up to 1 year

A: Restrict to ≤4 weeks where possible.

18
Q

also bzds are drvng rskk

19
Q

benzo overdose ???

20
Q

barbiturate mechanism ? whats it the same as
Q: Barbiturates MOA at inhibitory and excitatory receptors?

A

same moa as benz ut diff binding sites
A: Potentiate GABA-A and inhibit AMPA receptors.

21
Q

How are barbiturates “similar but different” to benzodiazepines?
A: Same overall pathway (enhance GABA-A), but different binding site

22
Q

: Why were barbiturates largely replaced by benzodiazepines?
A: Safety (narrower safety margin; more dangerous in overdose/with interactions) — hence rarely used as anxiolytics/hypnotics now

A

Any remaining barbiturate uses to recognise?
A: Intermediate-acting: only in severe intractable insomnia in patients already taking barbiturates (avoid elderly). Phenobarbital: still useful in epilepsy (sedative use unjustified). Thiopental: anaesthesia.

23
Q

whagts a barbturate stll used

A

Very short acting barbituate thiopental sodum used for anaesthesa

24
: Buspirone: does it work via GABA like BDZs? What class
A: No — it has no GABA effect, so it’s less sedating (“anxioselective”). AZAPIRONES
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Buspirone receptor MOA? A: 5-HT1A agonist at presynaptic autoreceptors initially → ↓ 5-HT release; over time autoreceptors desensitise → ↑ serotonergic firing/5-HT release.
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Q: Buspirone onset (important counselling)? A: Delayed: ~2–4 weeks to full effect. Anxiolytics, Sedatives Hypnoti… Q: Buspirone indication (per slide) and prescribing context? A: Oral medication for anxiety in adults (licensed short-term; can be extended under specialist management). Anxiolytics, Sedatives Hypnoti… Q: Buspirone key contraindication-type issue to anticipate clinically? A: CYP3A4 interactions: dose adjust with inhibitors (e.g., itraconazole, erythromycin) or inducers (e.g., rifampin, carbamazepine). Anxio
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Slide 26 — Acute vs chronic anxiety therapeutics LO Flashcards Q: Acute anxiety management drugs (per slide)? Q: Chronic anxiety (>4 weeks): what class becomes appropriate and why might BDZ be temporary add-on?
A: Benzodiazepine or buspirone. A: FOR CHRONIC ANXIETY Antidepressants (e.g., SSRIs/SNRIs/SARIs); BDZ may bridge until antidepressant takes effect.
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Slide 27 — SSRIs as anxiolytics (delayed; possible mechanism) LO Flashcards Q: SSRI counselling point about timing in anxiety? A: Delayed effect (about 3–4+ weeks). Anxiolytics, Sedatives Hypnoti… Q: Slide’s proposed “why SSRIs can reduce anxiety” (high yield wording)? A: 5-HT2C signalling can be anxiogenic; SSRIs may downregulate 5-HT2C and increase inhibitory GABA signalling in the amygdala.
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ide 28 — SSRI core MOA (e.g., citalopram/fluoxetine) LO Flashcards Q: SSRI MOA in one line? A: Inhibit serotonin transporter (SERT) at presynaptic terminal → ↑ 5-HT in synaptic cleft → prolonged postsynaptic receptor stimulation. Anxiolytics, Sedatives Hypnoti… Slide 29 — SARI (t(r)azodone) MOA + indications + timing LO Flashcards Q: Trazodone (SARI) indication in this deck? A: Approved/licensed for anxiety; can help insomnia. Anxiolytics, Sedatives Hypnoti… Q: Trazodone MOA (per slide wording)? A: Antagonist at 5-HT2A, agonist at 5-HT1A, and reuptake inhibition → increases available serotonin while blocking receptors contributing to anxiety/insomnia. Anxiolytics, Sedatives Hypnoti… Q: Trazodone time course (counselling)? A: May have immediate benefit for insomnia/anxiety; 2–4 weeks for depression effect. Beta-blockers (somatic anxiety) Slide 30 — Anxiety with palpitations/sweating/tremor (beta-blockers) LO Flashcards Q: Beta-blockers are used for which “type” of anxiety symptoms? A: Somatic/sympathetic symptoms: palpitations, sweating, tremor (performance-type physical symptoms). Q: Examples from LO list? A: Atenolol, propranolol. Anxiolytics
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SUMMARY CARD IMPORTANT Ultra-high-yield LO Flashcards (condensed “exam set”) Benzodiazepines (diazepam, temazepam) Q: BDZ MOA site + effect? A: +Allosteric modulator at GABA-A (γ subunit) → ↑ frequency of Cl⁻ channel opening → neuronal inhibition. Anxiolytics, Sedatives Hypnoti… Q: Indications? A: Severe anxiety short-term (2–4 weeks); some BDZs for insomnia (e.g., temazepam). Anxiolytics, Sedatives Hypnoti… Q: Adverse effects you must counsel? A: Sedation, hypnosis (dose-related), anterograde amnesia, reduced muscle tone, dependence/withdrawal. Anxiolytics, Sedatives Hypnoti… Q: Withdrawal facts? A: Anxiety most common; insomnia/depression/perceptual sensitivity; rare psychosis/convulsions; taper slowly. Anxiolytics, Sedatives Hypnoti… Z-drugs (zopiclone) Q: MOA (what receptor system)? A: Acts at benzodiazepine receptor on GABA-A to enhance inhibition (sedative–hypnotic). Anxiolytics, Sedatives Hypnoti… Q: Indication? A: Short-term insomnia. Anxiolytics, Sedatives Hypnoti… Barbiturates Q: MOA? A: Potentiate GABA-A + inhibit AMPA. Anxiolytics, Sedatives Hypnoti… Q: Why rarely used as anxiolytic/hypnotic now? A: Safety concerns; replaced by BDZs. Q: Remaining uses? A: Phenobarbital (epilepsy), thiopental (anaesthesia), rare severe insomnia in existing users. … SSRIs (citalopram) Q: MOA? A: SERT inhibition → ↑ synaptic 5-HT. Anxiolytics, Sedatives Hypnoti… Q: Anxiety counselling pearl? A: Delayed onset ~3–4+ weeks. SARIs (trazodone) Q: MOA? A: 5-HT2A antagonism + 5-HT1A agonism + reuptake inhibition. … Q: Indication/timing pearl? A: Licensed for anxiety; may help insomnia quickly; depression response takes weeks. Beta-blockers (atenolol, propranolol) Q: Indication in anxiety? A: Physical symptoms: palpitations, sweating, tremor.
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Clinical 1 — Acute severe anxiety, wants instant relief (important) A 23-year-old has severe acute anxiety with panic symptoms, asks for something that works today. Which is most appropriate from this lecture’s drug set? A. Citalopram B. Buspirone C. Diazepam D. Trazodone E. Atenolol
Best answer: C. Diazepam Why: Benzodiazepines give rapid anxiolysis (short-term use). … Why others are wrong: A/B: delayed onset (weeks). D: can help sleep/anxiety but not the classic immediate “abort severe anxiety now” choice in this set. E: targets somatic symptoms only, not core anxious distress.
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important Clinical 2 — Insomnia with “morning hangover” concern A 41-year-old needs short-term insomnia treatment and is terrified of morning grogginess. Which property best matches a hypnotic benzodiazepine approach? A. Long half-life active metabolites B. Rapid absorption + short duration + inactive metabolites C. Irreversible receptor binding D. Requires weeks for effect E. Blocks AMPA receptors
Best answer: B A would increase hangover; D is SSRI/buspirone-type; E is barbiturate feature.
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linical 3 — Dependence risk / stopping plan A patient has taken diazepam daily for 6 months. They want to stop immediately “cold turkey.” Best advice? A. Stop abruptly; withdrawal is mild B. Switch to zopiclone abruptly C. Gradual taper over weeks; may take months in some D. Add citalopram and stop BDZ same day E. Replace with phenobarbital for safety
est answer: C (gradual withdrawal, 4–8 weeks typical; sometimes much longer
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Clinical 4 — Anxiety with tremor/palpitations before a presentation A 20-year-old with no major psychiatric history has shaking hands, sweating, palpitations before OSCEs. They want something for the physical symptoms. A. Propranolol B. Temazepam C. Diazepam D. Citalopram E. Buspirone
est answer: A (licensed for somatic symptoms like tremor/palpitations/sweating
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Clinical 5 — Epilepsy link (barbiturate recognition) Which barbiturate is specifically noted as still valuable in epilepsy? A. Thiopental B. Phenobarbital C. Zopiclone D. Citalopram E. Trazodone
Best answer: B. Phenobarbital