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Psychiatry > Anxiolytic and Hypnotic Drugs > Flashcards

Anxiolytic and Hypnotic Drugs Flashcards

1
Q

How prevelant are anxiety disorders

A

seen in 28.8 % populaiton in lifetime with 4% at any one time

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2
Q

Define GAD

A

• Generalized persistent anxiety for at least 1 months duration.

Absence of the specific symptoms and patterns that characterize other anxiety disorders such as phobias, panic attacks or obsessive-compulsive disorder.

Psychological correlates include apprehensive expectation with worry fear and anticipation of misfortune to self and others, hyperattentiveness, distractibility, difficulty in concentrating, insomnia, feeling on edge and impatience.

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3
Q

How does the ANS respond to anxiety?

A
  • Sweating
  • Tachycardia and palpitations
  • Cold clammy hands
  • Dry mouth and lump in throat feeling
  • GI upset
  • Frequent urination and diarrhea

Voluntary Muscle Activation

•Jitteriness and an inability to relax

Complications - Abuse of alcohol, sedatives and antianxiety medications are common

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4
Q

____ has a role in slow wave sleep while ____ has a role in REM sleep

A

seratonin

Nepi

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5
Q
  • ______ - disorders of initiating and maintaining sleep.
  • ______ - disorders of excessive sleep or sleepiness.
A

Insomnia

Hypersomnia

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6
Q

Recommended tx for anxiety and insomina

A

• BENZODIAZEPINES and related drugs

  • SSRIs are commonly used
  • BUSPIRONE
  • CLASSICAL ANTIHISTAMINES

• ALCOHOL, CANNABIS, OPIATES • BARBITURATES

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7
Q

Whats going on in the GABAergic synapse?

A

Uptake of glutamate; takes excitatory NT in brain to make the inhibitory NT

GABA is released, binds ot GABA receptors:

GABA-A key in anxiety

GABA-B in msl relaxants

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8
Q

Where in the brain is GABA localized?

A
  • Substantia Nigra
  • Globus Pallidus •Hippocampus
  • Limbic structures - Amygdala
  • Hypothalamus
  • Spinal cord
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9
Q

Describe structure of GABA receptor

A

Has 5 units with 4 groups per unit

forms pore for Cl- to come in, enters and HYPERPolarizes and inhibits

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10
Q

describe interaction of Benzos on the GABA receptor

A

Binds to the Gamma subunit and enhances the action of GABA thus increase the Cl-release

works by INCREASING FREQUENCY of opening

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11
Q

What is the interaction of Barbituates on the GABA receptor?

A

They bind in allosteric site and increase duration of Cl- Channel opening

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12
Q

___ is the primary site of alcohol action and inhilation anesthetics

A

GABA

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13
Q

DIAZEPAM, ZOLPIDEM are examples of

A

Bensodiaezepines (work on GABA receptor)

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14
Q

What is the antagonist that would block benzos at their site of action on a GABA receptor?

A

Flumazenil

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15
Q

Partial agonist for 5-HT 1A - inhibition of adenylate cyclase and opens K+ channel

Also binds to dopamine receptors.

A

Buspirone

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16
Q

List of Benzos to tx anxiety

A
  • Alprazolam (Xanax®)
  • Diazepam (Valium®)
  • Lorazepam (Ativan®)
  • Clonazepam (Klonopin®) •Chlordiazepoxide (Librium®, Limbitrol®) •Clorazepate (Tranxene®)

•Oxazepam (Serax®)

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17
Q

Alprazolam

mechanism:

CNS effects:

Uses

A

GABA enhancement

Forebrain depression, dependence

Anxiolytic, antipanic

(short half)

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18
Q

Diazepam

CNS effects

mechanism

uses

A

Broad CNS depression, see dependence

GABA enhancement

anxiolytic, sedative, muscle relaxant

Long 1/2

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19
Q

Buspirone

Mechanism

CNS effects

Uses

A

5-HT effect

Little sedation, no dependence

Anxiolytic

delayed effect

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20
Q

What two antioxlytics are used as hynotics, what;s their differences?

A

Flurazepam: rapid onset, lasts long time

Triazolam: rapid onset, last SHORT

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21
Q

What is the role of lipophilicity in Diazepam

A

Fast onset, oral drug

has HIGH solubility thus quick to brain with rapid distribution in one dose

active metabolites change this in mult dose setting

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22
Q

Role of lipophilicity in Lorezepam (sleep and anxiety)

A

less lipophilic then diazepam with slower onset of action

longer duraion of action after single dose

no active metabolites

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23
Q

what are the only two drugs given at their active metabolite?

A

Lorezepam and Oxazepam

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24
Q

What are teh CNS effects of Benzos?

A
  • Decreased Anxiety
  • Sedation
  • Hypnosis
  • Muscle Relaxation
  • Anterograde Amnesia - IV administration
  • Anticonvulsant Action
  • Minimal CV and respiratory actions at therapeutic doses.
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25
Q

What drug interactions do we need to be aware of when prescribing benzos?

A
  • Produce additive CNS depression with most other depressant drugs such as ethanol, other sedative hypnotics and sedating antihistamines.
  • Drugs that affect hepatic metabolism such as cimetidine
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26
Q

Clincal uses of Benzos

A
  • Anxiety States
  • Sleep Disorders
  • Muscle Relaxant - diazepam
  • Seizure Treatment
  • Intravenous Sedation and Anesthesia
  • Alcohol Withdrawal - chlordiazepoxide

• Acute manic episodes - clonazepam

27
Q

What benzo is used for alcohol withdrawl?

A

Chlordiazepoxide

28
Q

What are the recommended benzos to tx anxiety

A

•Diazepam •Chlordiazepoxide •Alprazolam •Lorazepam •Clonazepam

29
Q

What signs do we need to be aware of in pt with benzo use that is in withdrawl

A
  • ANXIETY
  • INSOMNIA
  • IRRITABILITY
  • HEADACHE
  • HYPERACUSIS
  • HALLUCINATIONS

• SEIZURES

**Gradual dose reduction. Switch to longer acting drugs.

30
Q

High affinity for 5-HT1A receptors

Less sedating than benzodiazepines

No cross-tolerance with benzodiazepines

Does not potentiate other sedative-hypnotics and depressants

nor suppress symptoms of their withdrawal

Used in the treatment of generalized anxiety syndrome.

Therapeutic effects may take 1 to 2 weeks to occur

A
31
Q

What are some other tx for anxiety

A
  • SSRIs AND SNRIS- panic attacks and Generalized Anxiety Disorder - GAD
  • Beta-blockers - performance anxiety
  • Other sedatives - rarely
32
Q

What are the different dimensions of insomnia

A
  • Symptoms may be mild or severe. Transient, chronic or intermittent.
  • Can’t fall asleep and/or stay asleep.
  • Daytime sequelae: tired, fatigued, sleepy, anxious, depressed
33
Q

What benzos are used to tx insomnia

A

Flurazepam, Triaxolam, zolpidem, zaleplon and eszopiclone

34
Q

Benzo used as hypontic with rapid onset of action and long duration of action

A

Flurazepam

35
Q

Affects of Benzos on Sleep

_______latency to sleep

_____in stage 1 and 2 sleep;_____ time in stage 3 and 4and REM sleep

**Rebound insomnia upon withdrawal

A

Decreased

Increases, decreased

36
Q

What are some adverse effects to treating insomnia with benzos?

A
  • Daytime sedation
  • Ataxia
  • Rebound insomnia
  • Tolerance and dependence
  • Occasional idiosyncratic excitement and stimulation
37
Q

Non-Benzodiazepines chemically.

Bind to BDZ receptor on GABA receptor complex.

Weak anxiolytic, muscle relaxant and anticonvulsant at hypnotic dose.

A

Zolpidem (Ambien®) and Zaleplon (Sonata®)

38
Q

What effect does Zolpidem and Zaleplon have on Stages of sleep

A

Stage 3 and 4 sleep preserved, minor effects on REM sleep. Zolpidem typical duration of action 5-6 hours. Sustained release preparation now available. Duration of action 7 to 8 hours. Now also available as an oral spray targeted at problems of sleep initiation and sublingual tablets for middle of the night waking.

39
Q

is a hypnotic agent that is similar to zolpidem with a faster onset of action and a shorter terminal elimination half- life compared to zolpidem.

A

Zaleplon

40
Q

zolpidem (ambien) and Zalepon are Antagonized by

A

flumazenil

41
Q

Similar in mechanism to zolpidem and zaleplon.

Is thought to act through an interaction with the GABA-receptor complex at binding domains located close to or allosterically coupled to the BDZ receptor.

Approved for use for six months based on drug company studies.

• Low likelihood of dependence and withdrawal. DEA schedule IV drug.

A

Eszopiclone - Lunesta

42
Q
  • melatonin MT1 and MT2 receptor-agonist.
  • It is specifically indicated for the treatment of insomnia characterized by difficulty in falling asleep. It is not a controlled substance.
A

Ramelteon - Rozerem

43
Q

Secobarbital and Phenobarbital are both

A

Barbituates: huge OD issue and used in death penalty

44
Q

Barbituates are

  • ______ absorbed and distributed.
  • Highly lipid soluble compounds such as thiopental distribute rapidly to brain. Action terminated by______,
A

Rapidly

redistribution

45
Q

What is special about barbituate metabolism?

A

Can induce own metabolism and that of other drugs. • Eliminated primarily by renal excretion.

46
Q

What are the CNS effects of Barbituates

A

Sedation, Hypnot action, Anesthesia

***Respiratory distress

High dose causes sustained decrease in mean arterial and pulse pressure

induction of hepatic metabolism

47
Q

Do we see tolerance or physical dependence in Barbituates?

A

see metabolic and pharmacodynamic tolerance as well as physical dependence; pts will have symptos of withdrawl such as anxiety, aggitation, insomnia, tremo and life threatening seizures

48
Q

What happesn in acute poisoning from barbituaties

A

stupor, coma and respiratory distress

49
Q

What kind of drug interactions do we see in Barbituates?

A
  • Additive with other CNS depressants such as alcohol, other sedative hypnotics and antihistamines.
  • Drugs that affect microsomal drug metabolism
50
Q

Short to intermediate acting barb with moderate lipid solubioity and onset of 10 mins; treats insomnia, lasts 3-4 hrs

A

Secobarbital

51
Q

Long acting barb with low lipid solubility, takes 60 mins to work, lats 10-12 hrs and is for seizures and insomnia

A

Phenobarbital

52
Q

Ultrashort acting barb with High lipid solubility, onse it 30 secs and lasts for 12 mins for induction of anesthesia, or seizure tx

A

thiopental

53
Q

Aldehyde hydrate with pungent taste and somewhat caustic taste.
a. Metabolized to trichloroethanol which is the active form of the drug.

b. Pharmacology similar to barbiturates.
c. Less effects on stages of sleep than benzodiazepines and barbiturates.

A

Chloral hydrate

54
Q

• New hypnotic approved 2014.

Orexin receptor (OX1 and OX2) antagonist. Orexins are neuropeptide central promoters of wakefulness through excitement of brain regions involved in arousal and attention

A

Suvorexant

55
Q

Drugs used to reduce muscle tone associated with spasticity related to multiple sclerosis injuries and other muscular skeletal disorders

A

SKELETAL MUSCLE RELAXANTS

56
Q

is characterized by increases in tonic stretch reflexes and flexor muscle spasms, together with a possible muscle weakness

A

Spasticity

57
Q

Mech of Spasticity

A

Mechanisms underlying spasticity involve both the stretch reflex arc itself and higher centers in the brain.

Pharmacological treatment of spasticity targets both sites.

58
Q

GABAergic agents as muscle relaxants

A

Diazepam and Baclofen

59
Q

Its action in reducing spasticity is at least partly mediated in the spinal cord.

It can be used in patients with muscle spasm of almost any origin including local trauma.

It produces sedation in most patients at the doses required to reduce muscle tone.

A

Diazepam

60
Q

GABA-mimetic agent that works at GABAB receptors. This results in hyperpolarization, causing presynaptic inhibition.

This can result in decreased release of excitatory transmitters such as glutamate.

is at least as effective as diazepam in reducing spasticity and produces much less sedation.

A

Baclofen

61
Q

_____ interferes with releaes of excitatory transmitters

_____ facilitates GABA mediated presynpatic inhibition

A

baclofen

diazepam

62
Q

an alpha2 - adrenergic agonist that is related to clonidine. It may enhance both presynaptic and postsynaptic inhibition.

A

Tizanidine

63
Q

Efficacy of Tizanidine compared to Diazepam and Baclofen

Side effects

A

May have similar efficacy to diazepam and baclofen in relieving muscle spasm.

Side effects include drowsiness, hypotension, dry mouth and asthenia.

64
Q

Tizanidine interacts with

A

Interacts with ciprofloxacin and fluvoxamine (CYP1A2 inhibitors)

Psychiatry (19 decks)

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