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BMB > Anxiolytics, Sedatives And Hypnotics > Flashcards

Anxiolytics, Sedatives And Hypnotics Flashcards

1
Q

Benzodiazepines

A 
Aprazolam
Chlordiazepoxide
Clonazepam
Diazepam
Lorazepam
Midazolam
Temazepam
Oxazepam
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2
Q

BZD antagonists

A

Flumazenil

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3
Q

Azapirones

A

Buspirone

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4
Q

Miscellaneous insomnia medications

A

Zolpidem
Zaleplon
Eczopiclone
Suvorexant

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5
Q

Melatonin receptor agonist

A

Remelteon

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6
Q

General effects of CNS depressants as a function of dose

A 
Anxiolysis 
Sedation
Hypnosis
General anesthesia
Death- depression of medulla with resp. Suppression

*effects predominantly driven by dose

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7
Q

GABA cycling

A

Following neuronal release of GABA, it is transported to the nerve terminal by GAT-1 or transported to Astro Yates
Intracellularly, GABA is metabolized to glutamine and succinate by GABA aminotransferase in the astrocyte

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8
Q

Site of drug action

A

Complex, distinct binding to GABA-A receptor domain

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9
Q

Agonist activities at BZD receptor

A

Anxiolytic, sedative/hypnotic, muscle relaxant, anticonvulsant, amnestic dependency

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10
Q

Partial agonist activity at BZD receptor

A

Anxiolytic only

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11
Q

Partial inverse agonist

A

Promnestic (memory) enhancing

anxiogenic

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12
Q

Inverse agonist activity at BZD receptor

A

Promnestic
Anxiogenic
Pro-convulsants

*affects receptors that have constitutive activity and decrease the baseline level of activity. Receptor will still bind to an agonist or antagonist, but just modulates its baseline activity.

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13
Q

Clinical uses of benzodiazepine

A 
Anxiety disorders
Insomnia
Seizure disorders
Agitation or anxiety association with other psychiatric disorders
Pre-operative amnestic
Alcohol withdrawal
Spastic disorders 
Involuntary movement disorders
Sedation- pre procedural, during mechanical ventilation in critically ill patients
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14
Q

BZD are cross tolerant with

A

Alcohol

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15
Q

BZD and anxiety - adv/disadv

A

Selection is not driven by efficacy- all same efficacy in both acute and chronic anxiety. Driven by pharmacokinetics- side effect profiles

Adv- rapid onset, relatively safe, good tolerability- no activation, useful for breakthrough symptoms, may enhance adherences to Tx and alleviate activation Sx of SRRIs (worse anxiety when first start SSRI)
Disadv- no reliable antidepressant efficacy, limited spectrum of efficacy, BID/TID dosing, initial sedation, possibility of physiologic dependence, risk of w/d sx upon discontinuation, concern regarding abuse potential (polysubstance abusers, lower probability in anxious patients without substance abuse)

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16
Q

BZD structure

A

Structure activity relationships- all have 1,4-benzodiazepine ring system. Modification of the ring system results in differential electron-attracting ability of the attachment at the R1 position and increases potency
Tolerability comes into play here

17
Q

BZD absorption

A

Rapidly absorbed BZD enter the circulation quickly

GI absorption is dictated by intrinsic properties of the BZD

18
Q

Liposolubility and BZD

A

Lipophilicity, at physiologic pH influences the rate at which it crosses the BBB by passive diffusion and this in turn influences the speed of onset of action and intensity of effect
Highly lipophilic BZD enter the brain more quickly, ‘turning on’ the effect promptly, but ‘turning off’ the effect more quickly as they disappear into the fat
Less lipophilic compounds like lorazepam produce clinical effects more slowly but may provide more sustained relief, in spite of a shorter half life

19
Q

BZD duration of action

A

Determined by rate and extent of distribution rather than by the rate of elimination
Less lipophilic agents maintain their effective CNS concentrations longer because they are less extensively distributed to the periphery

20
Q

BZD biotransformation

A

BZD are metabolized hepatically by microsomal oxidation or glucuronide conjugation
Oxidative pathway is influenced by hepatic disease, age, several illnesses and the presence of other drugs that affect ox capacity- magnify the side effects of BZD
BZD that are conjugated are safer than those that are metabolized by oxidation in the elderly and hepatic diseases (*midazolam will accumulate in those with hepatic diseases, specifically)

21
Q

3 BZD that are not oxidatively metabolized

A

No active metabolites and are just conjugated- shorter half life

Lorazepam, oxazepam, temazepam

22
Q

Metabolism of BZD- age

A

Age related decline in phase 1 metabolism- oxidative
Decreased clearance and increased half life for some medications (diazepam, piroxicam)
Phase 2 metabolism is unaffected by age- glucuronide conjugation
Decreased liver mass in elderly

23
Q

BZD drug interactions

A

CNS depressants- potentiate BZD-associated sedation
Cimetidine- inhibits metabolism of longer acting BZD
Fluoxetine- decreases clearance of diazepam
CYP3A4 inhibitors (fluoxetine, fluvoxamine, grapefruit juice, ketoconazole)- decreased clearance of alprazolam and midazolam as well as triazolam

24
Q

BZD tapering and symptoms of withdrawal

A

10% recommended reduction rate, gradually over a period of several weeks, withdrawal rate is often determined by a person’s capacity to tolerate symptoms
Same as symptoms for alcohol and barbiturate withdrawal- increased anxiety, nervousness, sleep disorders, inner restlessness, depressive symptoms, irritability, psychosis-like conditions, delirium, depersonalization/derealization, confusion
Autonomic symptoms- trembling, sweating, nausea, dyspnea, motor agitation, increased HR/BP, headache, muscle tension
Seizures are the defining component of delirium tremens phase
Neurological- cognitive impairments, hyperacusis, photophobia, hypersomnia, muscle twitching

25
Q

Factors that increase complications and difficulty associated with withdrawal

A

Pharmacological factors- higher daily dose, shorter half life, longer duration of prior BZD therapy, more rapid taper
Clinical factors- panic disorder, higher pre-taper levels of anxiety or depression, more personality psychopathology, concomitant substance abuse/use

26
Q

Treatment of BZD and alcohol withdrawal

A

Load with long-acting BZD
Monitor vital signs serially (HR, resp.)
Monitor alcohol withdrawal symptoms serially (tremulousness, mental status, diaphoresis)
BZD admin- scheduled and PRN BZD (when necessary) or continuous when delirium begins (usually lorazepam)

27
Q

BZD: sedation

A

Decreases pre-surgical anxiety: diazepam

Continuous infusion therapy for sedation- lorazepam and midazolam (only available IV, anterograde amnesia)

28
Q

BZD muscle relaxants

A

Decrease muscle spasms and pain associated with injury or trauma
Act at spinal and supraspinal levels, not at NMJ
Decreases spasticity
Required doses often result in excessive sedation
Clonazepam may be BZD of choice because of less sedation

29
Q

Flumazenal

A

Able to reverse a full agonist BZD acting at the BZD site of the GABAa receptor complex
This may be helpful in reversing the sedative effects of the BZD when administered for anesthetic purposes or when taken in overdose by a patient.
Do not give to patients who are chronically treated with BZD- seizure risk

30
Q

Non-benzo anxiety Tx

A

Buspirone- 5HT1A agonist, does not act at GABAA/BZD receptor complex
Does not exhibit cross tolerance with BZDs
Fewer and less severe CNS effects
Little dependence liability
Slow onset of action
1/4 as effective as BZD, 2/3 as effective as SSRI
Good adjuvant therapy with SSRI

31
Q

Insomnia drugs

A

Eszopliclone
Zolpidem
Zaleplon

32
Q

Zaleplon

A

Acts selectively at omega-1 BZD receptor site, involved in sedation
Not omega-2BZD site (concentrated in areas of brain regulating cognition, memory, motor function, etc.)
Rapid onset and half life is about 1 hour
Ideal for jet lag and for those who require complete wash out before morning
Some evidence of dependence
Class IV like other Z drugs
Low incidence of side effects- headache, constipation, difficulty with concentration, ataxia, dry mouth

33
Q

Zolpidem

A

Rapidly absorbed, quick onset of action
2.5 elimination half life
Weak anxiolytic properties
No incidence of AM hangover
Little amnestic response
Class IV
Multiple formulations with varying release properties
Low incidence of side effects- daytime drowsiness, dizziness/vertigo, ataxia, diarrhea
*reduced dosing in women secondary to decreased clearance

34
Q

Eszopiclone

A

Presumed moa results from an interaction with GABA receptor complexes at binding domains located close to or allosterically coupled to BZD receptors
Non-BZD hypnotic that is pyrrolopyrazine derivative of the cyclopurrolone class with a chemical structural unrelated to pyrazolopyrimidines, imidazopyridines, BZDs, barbiturates, or other hypnotics.
Unique in that safety and efficacy data exist at 6 months
Alcohol and drugs with sedating effects should not be used with eczopiclone since their sedating effects are additive
Sedation, dizziness, risk of dependence are SEs

35
Q

Suvorexant

A

Novel dual orexin receptor antagonist (orexin in lateral hypothalamus and goes to diffuse NT systems for arousal and vigilance, levels are low in narcolepsy)
Prevents arousal and promotes sleep
Approved for tx of insomnia
Improved sleep latency, wake after sleep onset, total sleep time
Contraindicated in patients with narcolepsy
In obese women, increase Cmax and AUC- side effects will be longer, use lower dose

36
Q

Neuropsychopharmacology of insomnia in pediatric population

A

Alpha 2 agonists- guanfacine, clonidine (decrease presynaptic calcium entry and decrease noradrenergic and DA NT release in prefrontal)= sedative effects

37
Q

Barbiturates

A

Phenobarbital
Because of dependency and withdrawal symptoms and a lack of favorable safety profile, especially with other drugs, they fell out of favor
Variability of action and duration
Many active and inactive metabolites that are hard to predict
Lethal in overdose
Used in some refractory epilepsy

BMB (10 decks)

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