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Mental Health > Anxiolytics > Flashcards

Anxiolytics Flashcards

1
Q

Sedative (anxiolytic) agents

A

Agents that reduce anxiety and exert a calming effect

Must be very careful with these agents since they exist on a dose-dependent continuum that includes hypnosis, anesthesia, coma and death

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2
Q

Hypnotic agents

A

Produce drowsiness and encourage onset and maintenance of a sleep state

Must be very careful with these agents since they exist on a dose-dependent continuum that includes hypnosis, anesthesia, coma and death

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3
Q

What is the overarching guiding principle for prescribing a sedative and hypnotic agents

A

Minimize the dose as best as possible to gain therapeutic effect
- minimize CNS depression

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4
Q

What is the dose:degree of CNS depression relationships for barbiturates and alcohol?

A

It is a linear, positive correlation
- there is a direct correlation between size of dosage and CNS depression

the more you take of this medication in one sitting, the greater chance you have of coma or death

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5
Q

What is the dose:CNS depression relationship for benzodiazepines and newer hypnotic agents

A

Tapered linear positive correlation
- show the same linear correlation as barbiturates and alcohol, but the slope decreases at around anesthesia level

the more you take of this drug, the quicker you can get to anesthesia, however it requires massive OD to get to coma/death (so more safer)

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6
Q

Indications for anxiolytic/sedative and hypnotic agents

A

GAD

PTSD

Acute stress disorder

Panic disorder

Obsessive compulsive disorder

Sleep-wake disorders ( hypnotic and sedative only)

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7
Q

Neurochemical theories of anxiety

A

Are a result of an over activity of brain mechanisms of responses to threats
- avoidance/hyper vigilant/ increased arousal

Anxiety disorders exist on spectrum
- also comorbidity between disorders is common (often have multiple, especially with severe anxiety)

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8
Q

Anxiety generalized spectrum

A

Mild = simple phobias and social phobias

Moderate = GAD/PTSD via simple trauma

Severe = panic/agoraphobia, depression and social phobias combined, PTSD from multiple trauma

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9
Q

Why do people with chronic moderate-severe anxiety often show hyporeactive to simple startle stimuli?

A

They are sensitized to startle stimuli, so it takes a larger than normal startle to actually gain a hyper reactive or even normal response
- their “normal” baseline is higher than normal

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10
Q

What is the chief neurotrophic peptide that is responsible for a acquisition and extinction of anxiety?

A

BDNF

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11
Q

Noradrenergic model of anxiety

A

ANS of anxious patients are hypersensitive to stimuli
- chronic over activity of NE release from the locus coeruleus

Chronic NE release leads to downregulation of a2 adrenergic neurons (since they are chronically being activated by NE)
- this is what is seen in GAD patients

Therefore, anxiolytic drugs act on inhibiting the firing of the locus coeruleus release of NE

also administration of anxiogenic agents (a2-antagonists) causes increased NE release form locus coeruleus and results in anxiety and panic attack as ADRs

** also explains by BBs are used in anxiety patients to limit peripheral effects of mass NE release**

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12
Q

GABA-receptor model of anxiety

A

GABA signaling inhibits 5-HT, NE and dopamine systems
- GABA(a) specifically is targeted for anxiety reduction and sedation

Number of GABAa receptors can change with environment and the subunit expression can be altered by hormones
- this is why alcohol withdrawal results in anxiety as one of the early symptoms

benzos enhance the GABAa receptor (allosteric modulators, NOT agonists)

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13
Q

Serotonin model of anxiety

A

There is mixed evidence of either increased or decreases 5-HT levels in anxiety patients

It is believed that enhancing 5-HT activity will reduce NE activity in the locus coeruleus

  • reduces CRF and cortisol and defense/escape responses
  • SSRIs increase 5-HT levels by blocking manifestations of panic and anxiety

however, agonists for 5-HT1a receptors, work for GAD but actually can make panic disorders worse or not work at all

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14
Q

Benzodiazepines “epam’s”

A

Are (+) allosteric modulators for GABA(a) receptor

  • THEY ARE NOT AGONISTS
  • enhances endogenous GABA signaling

Indications

  • anxiety
  • status epilepticus (diazepam only)
  • seizures
  • alcohol withdrawal
  • insomnia
  • preansethetic medications
  • Meniere disease (diazepam only)

Metabolism

  • metabolized by CYP 3A4 and 2C19 in the liver
  • diazepam, chlordiazepoxide and prazepam are broken down first into ozazepam before excreted (so if giving these agents, need to be aware your essentially giving 2:1)
  • longer half-life benzos = decreased likelihood of withdrawl

ADRs:

  • Drowsiness
  • rebound insomnia
  • confusion
  • ataxia (only at high doses)
  • withdrawal and OD symptoms

very easy to abuse so must monitor

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15
Q

Long-term benzo use

A

If used longer than 2 weeks, need to taper dose or switch to a longer half-life compound and decrease from there

  • ease withdrawal symptoms
  • NEVER quit cold turkey

triazolam can also cause amnesia and respiratory failure if not tapered well (almost never used because of this)

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16
Q

Withdrawl/OD benzo Symptoms

A

Anxiety

Irritability

Insomnia

Tremors

Hyperasthesia

Myoclonic seizures

Delirium

  • while ODing by itself is super rare (with alcohol = more common), withdrawl immediately is often fatal*
  • must give flumazenil in conjunction to help prevent
17
Q

Barbiturates “barbital’s”

A

(+) allosteric modulators at GABAa receptors = LOW DOSES

Agonists of GABAa receptors = HIGH DOSES

  • hence why fatal ODing is wayyy more common than benzos*
  • also withdrawl symptoms are almost always fatal

Very limited scope of use in medicine because of abuse potential and easiness to kill self if not used properly

18
Q

Buspirone

A

5-HT(1a) agonist

Indications
- GAD and anxiety
(especially in the elderly and chronic cases)
- anxiety with MDD
(must be given conjunction with SSRI in this case)

Takes 2-4 weeks to actually take effect usually

ADRs:

  • relatively mild except sedative effects
  • low chance of abuse (but still possible)
  • doesnt interact with alcohol*
19
Q

Chloral hydrate

“Knock out drops”

A

Used mainly only to treat patients with paradoxical reactions to benzos

Acts similar to barbiturates, however is metabolized by alcohol dehydrogenase (competes with alcohol, so NEVER mix)
- also skips CYP system

20
Q

Meprobamate and carisoprodol

A

Anxiolytic agent that is most commonly used for short-term relief of anxiety only

  • is a tranquilizer
  • also produces mild analgesic effects

ADRs:

  • CNS depression and respiratory depression (large doses)
  • hypotension
  • shock and heart failure (large doses)
  • enhances analgesic effects and CNS depression of other drugs

doesnt mix with alcohol well

Carisoprodol = skeletal muscle reactant that gets metabolized into meprobamate

21
Q

What is the common treatment action for severe acute anxiety

A

1) initially give a benzo (i.e lorazepam) with a SSRI/SNRI(escitalopram)
2) once the SSRI/SNRI has reached therapeutic levels for a week or so, begin tapering off the benzo slowly by either slowly reducing the dose currently or switching to long acting benzo and taper from there (this preferred)
* remember that SSRIs and SNRIs take a few weeks to kick in, whereas benzos act immediately*

22
Q

Types of insomnia

A

1) Transient insomnia: <3days
- brief environmenal or situational stressor is the cause
- lowest dose of hypnotics treats this
- DONT give benzos for this if an important life event is about to occur since they often impair performances.

2) short-term insomnia: 3 days- 3 weeks
- personal stressor is usually the cause
- hypnotics may be used adjectively and intermittently for 7-10 nights

3) long-term insomnia: > 3 weeks
- specific stressor that is often not identifiable until psychiatric consultation is done
- requires multi approach for treatment which includes hypnotics

23
Q

Hypnotic effects

A

Hypnotics reduce sleep latency but disrupt sleep architecture

  • dose-dependent decrease in REM and N1/N2 sleep
  • barbiturates > benzos> newer agents and Z-drugs

Next day ADRs:

  • rebound anxiety
  • continued sedation on mental depression
  • dysphoria
  • amnesia (benzos only)

Chronic use ADRs:

  • rebound insomnia with cessation (builds tolerance of drug)
  • dependence and withdrawal
24
Q

What are the approved benzos for insomnia?

A

Flurazepam, temazepam, quazepam, estazolam

25
Q

Benzodiazepine receptor agonists

“Z-drugs”

A

Includes zolpidem and zaleplon

Actually act as an agonist at the benzo receptor on GABAa receptors

  • not structurally similar to benzos and only work for insomnia (sedative effects only)
  • low disruption in sleep architecture

There is no anticonvulsant, anxiolytic or muscle relaxants effects

ADRs:

  • none specific and generally well-tolerated
  • doesn’t mix with alcohol well though

Mental Health (46 decks)

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