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PR3136 PT IV > Anxiolytics > Flashcards

Anxiolytics Flashcards

1
Q

what’s the difference between anxiety and fear

A 
anxiety = anticipated threat, vague
fear = present danger
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2
Q

similarities between fear and anxiety

A

the threat may be real or perceived

both responses: defensive behaviours, autonomic reflexes, arousal, corticosteroid production, negative emotions

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3
Q

Psychological manifestations of anxiety states

A
  • negative emotions: worry, nervousness, unease
  • arousal
  • lack of concentration
  • insomnia
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4
Q

Physical manifestation of anxiety states

A
  • tachycardia
  • SOB
  • nausea
  • gastric acid hypersecretion
  • trembling (skeletal muscles activated)
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5
Q

what is the biochemical basis that cause psychological and physical manifestation of anxiety states

A
  • central and peripheral noradrenergic/adrenergic activation –> flight or fight response
  • stress response –> HPA axis –> secretion of stress hormones (cortisol)
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6
Q

main anxiety disorder that is discussed in lecture

A

generalised anxiety disorder (GAD)

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7
Q

what is GAD?

A
  • excessive worrying over everyday matters
  • interferes w daily functioning
  • both psychological and physical manifestation
  • diagnosed when present for at least 6 months
  • most common cause of disability in the workplace
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8
Q

what are the 3 different therapeutic effects that can be seen in anxiolytic drug?

A

CNS depressant:

  1. sedative = cause sedation/relaxation but still aware
  2. hypnotic = induce drowsiness and sleep,may have amnestic effects
  3. anxiolytic = reduced anxiety
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9
Q

at what doses can i see the different types of therapeutic effect?

A
  1. low dose: anxiolytic, sedative effects
  2. higher dose: hypnotic
  3. even higher dose –> cause anaesthesia, used for surgery
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10
Q

which BZDs is used as anxiolytics /sedatives?

A

diazepam, lorazepam

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11
Q

which BZDs is used as hypnotics?

A

diazepam, triazolam, temazepam

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12
Q

which BZDs is used as pre-anaesthetics?

A

diazepam, midazolam

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13
Q

which BZDs used for anti-convulsant effect?

A

diazepam

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14
Q

MOA of BZDs

A

binds to the BZD site (allosteric site) away from the GABA site

potentiate GABA actions by increasing the frequency of GABA-induced channel opening

potentiates influx of CL- ions leading to greater hyperpolarization –> neurons not firing

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15
Q

what happens when the GABA is activated or potentiated in this case with BZDs?

A
  • alters mood via the limbic system
  • cause drowsiness via reticular activating system
  • relax muscles vis motor cortex
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16
Q

what are the short acting BZDs and their uses?

A

midazolam (anaesthetic), triazolam (hypnotic)

17
Q

what are the intermediate BZDs and their uses?

A

Temazepam (hypnotic), Lorazepam (anxiolytic/sedative)

18
Q

what are the long acting BZDs and their uses

A

diazepam
(anxiolytic/sedative, hypnotic, anaesthetic, status epilepticus (anti-convulsant)

  • longer acting for chronic conditions
19
Q

Adverse effects of BZDs

A
  1. acute toxicity/ overdose –> severe respiratory depression, esp w concurrent use of alcohol

–> treated w flumazenil, a benzodiazepine antagonist

  1. SE: drowsiness, confusion, amnesia
    - impaired muscle co-ordination (impair manual skills - cannot use machinery)
  2. tolerance: depends on freq of use
    - develops faster for epilepsy than for use to induce sleep
  3. dependence: withdrawal effect = disturbed sleep, rebound anxiety, tremor, convulsion
    - to withdraw GRADUALLY
    - has abuse potential
20
Q

What are the names of the non-BZDs

A
  • zolpidem
  • buspirone
  • barbiturates
  • pregabalin
  • hydroxyzine
  • propanolol
21
Q

MOA of Zolpidem

A
  • potentiates GABAa mediated CL- currents at the same site as BZD
22
Q

Therapeutic effects of zolpidem

A
  • good hypnotic effect: PRIMARILY used to treat insomnia

- NOT effective as an anxiolytic

23
Q

MOA of buspirone

A
  • serotonin 5-HT1A receptor partial agonist

- bind to dopamine receptors

24
Q

Therapeutic effects of buspirone

A
  • GAD, but anxiolytic effect takes 1-2 weeks

- lacks anti-convulsant and muscle relaxant properties

25
Q

MOA of barbiturates

A

potentiates the GABAa mediated CL- current, at barbiturate site (not at BZD site)

26
Q

Therapeutic effect of barbiturates

A
  • sedative-hypnotic BUT
  • NOT used freq due to higher tolerance and dependence compared to BZDs (barbiturates: directly proportional vs BZDs: increases and plateaus)
  • severe withdrawal symptoms
  • flumazenil not effective in treating barbiturate overdose
  • at anaesthetic doses (higher doses) –> e.g. phenobarbital can DIRECTLY open CL- channels and block Na+ channels
27
Q

3 different types of barbiturates

A
  • long-acting (1-2 days)
  • short (3-8hrs)
  • ultra-short (20min)
28
Q

therapeutic effect of long acting barbiturates?

A
  • anticonvulsant –> phenobarbital
29
Q

therapeutic effect of short acting barbiturates?

A

sedative & hypnotic –> pentobarbital, amobarbital

30
Q

therapeutic effect of ULTRA short acting barbiturates?

A

IV induction of anesthesia –> thiopental

31
Q

MOA of pregabalin

A
  • GABA analogue increases synaptic GABA –> GABA receptor mediated CL- current –> hyperpolarization
  • acts on voltage-gated Ca2+ channels
32
Q

SE of pregabalin

A
  • assoc w worsening of suicidal thoughts
33
Q

Therapeutic effect of pregabalin

A
  • treat GAD, also has anticonvulsant effect
34
Q

MOA of hydroxyzine

A
  • first gen antihistamine;
  • anxiolytic effect: antagonism of serotonin 5-HT2 receptors
  • activity on a-adrenergic receptors as well
35
Q

Use of hydroxyzine

A
  • low addictive potential (compared to BZD/barb)

- helps w itching and nausea manifestation of anxiety

36
Q

MOA of propanolol

A

BB: b-adrenergic receptor antagonist

37
Q

Use of propanolol

A
  • treat performance anxiety and social phobias

- reduce PHYSICAL symptoms assoc w adrenergic activation

38
Q

CI of propanolol

A

asthma and heart conditions

39
Q

Other anxiolytics names:

A

NaSSA: Mirtazapine

TCA: Clomipramine

SSRI: fluoxetine, citalopram, sertraline, paroxetine

SNRI: venlafaxine, duloxetine

PR3136 PT IV (17 decks)

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