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Neuro-pharmacology > Barbiturates > Flashcards

Barbiturates Flashcards

1
Q

Anxiolytic

A

Reducing anxiety or tranquilizing

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2
Q

Sedative

A

Calming, relaxing, or sleep inducing

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3
Q

Hypnotic

A

Sleep inducing or sopoforic

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4
Q

soporific

A

tending to induce drowsiness or sleep

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5
Q

Normal anxiety is a

A

survival response leading to activation of the
sympathetic nervous system for fight-or-flight response to danger

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6
Q

Anxiety is the

A

anticipation of potential danger

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7
Q

anxiety is the Subjective unsettling feelings of

A

concern or worry

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8
Q

Physiological responses of anxiety including

A

sympathetic activation

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9
Q

anxiety range

A

Ranges from vague discomfort to intense sense of terror

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10
Q

Acute anxiety in response to stressors can be

A

beneficial

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11
Q

Moderate anxiety for exams drives

A

studying

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12
Q

Anxiety for public speaking prompts

A

thorough preparation

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13
Q

Chronic or excessive anxiety can cause

A

deterioration of performance and
distracting preoccupation with the agitation associated with anxiety

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14
Q

Sympathetic effects of stress and anxiety

A

increased muscle tension, digestive problems, sleep disturbance

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15
Q

Escalating anxiety

A

cycle due to performance decrease and fear of failure (driving further
anxiety)

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16
Q

Anxiety has high comorbidity with depressive disorders and substance abuse 59%

A

of patients with major depressive disorder have a co-morbid anxiety disorder

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17
Q

Anxiety has high comorbidity with depressive disorders and substance abuse 20%

A

of patients anxiety/mood disorder patients have a comorbid substance abuse
disorder (esp. alcohol)

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18
Q

Rates of alcohol abuse highest with

A

social anxiety disorders

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19
Q

GENERALIZED ANXIETY
DISORDER (GAD)

A

Symptoms of anxiety without identifiable cause

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20
Q

GAD Persistent anxiety most of

A

each day for prolonged periods (weeks/months)

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21
Q

GAD Constant

A

worry, predicting, anticipating, or imagining failure or
disastrous events

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22
Q

physical symptoms of GAD (5)

A

muscle tension and agitation leading to
poor concentration, irritability, and sleep disturbances

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23
Q

PANIC ATTACKS / PANIC
DISORDER

A

Experiencing physiological effects of fear reactions without
threatening stimulus

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24
Q

PANIC ATTACKS / PANIC
DISORDER Accompanied by strong

A

sympathetic NS activation

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25
Q

PANIC ATTACKS / PANIC
DISORDER Accompanied by strong sympathetic NS activation

A

Increased heart rate, chest pain
* Sweating
* Shortness of breath, faintness
* Choking
* Fear of losing control or dying

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26
Q

Panic attack in response to a

A

cue can lead to phobia

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27
Q

Susceptibility for un-cued panic attacks leads to

A

panic disorder

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28
Q

Early anxiolytic and sedative hypnotic
drugs

A

alcohol & Bromides

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29
Q

Contemporary anxiolytic and sedative
hypnotics

A
  • Barbiturates
  • Benzodiazepines
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30
Q

Bromide toxicity

A

Bromides are sedative possibly through effects on Clbalance in the CNS

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31
Q

Bromides were the first effective

A

anticonvulsant

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32
Q

Bromides have the side effect of

A

decreased libido which coincidentally supported the prevailing notion (at the time) that epilepsy was caused by masturbation

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33
Q
  • Bromide has a half-life of
A

~8-12 days making dosing
difficult and intoxication problematic

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34
Q

Bromism results from

A

bromide toxicity

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35
Q

Bromism results from bromide toxicity (5)

A
  • Impaired thought and memory
  • Drowsiness, dizziness
  • Irritability, emotional disturbances
  • Repulsive skin eruption (rash)
  • Bromide psychosis (delirium, delusions, vivid
    hallucinations, mania, lethargy, and coma)
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36
Q

Barbital was the first

A

psychoactive barbiturate synthesized in 1903 and marketed as
Veronal

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37
Q

Barbital found to have

A

relaxing and sopoforic effects

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38
Q

Barbital Long half-life meant

A

drowsiness extended for days

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39
Q

Phenobarbital was developed in 1912 and was noted to be

A

faster acting, of shorter duration, and having excellent anticonvulsant properties

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40
Q

Barbiturates can be classed
according to the

A

relative
lipophilicity of the compound.

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41
Q

Increasing the lipophilicity of
barbiturates results in

A

n faster
uptake into the brain and more
rapid sedation

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42
Q

Effects of barbiturates low doses

A

Anxiolytic and
tranquilizing at low
doses

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43
Q

Effects of barbiturates moderate doses

A

Sedating and sopoforic

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44
Q

effects of barbiturate’s at high doses

A

Anesthetic at high doses

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45
Q

Ultrashort-acting barbiturates are

A

anaesthetic

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46
Q

Ultrashort-acting barbiturates are
anaesthetic - Highly

A

lipophilic

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47
Q

Ultrashort-acting barbiturates are
anaesthetic - names

A

Thiopental, hexobarbital

48
Q

Ultrashort-acting barbiturates are
anaesthetic - IV administration results in

A

rapid uptake and sleep in 10-20 seconds

49
Q

Ultrashort-acting barbiturates are
anaesthetic - Unconsciousness lasts ____ and
ends due to

A

20-30 minutes and
ends due to redistribution of lipophilic
barbiturates into fatty tissues

50
Q

Short/intermediate-acting barbiturates
are

51
Q

Short/intermediate-acting barbiturates
are sedative - Moderate

A

lipid solubility

52
Q

Short/intermediate-acting barbiturates
are sedative - names

A

Amobarbital (Amytal) and pentobarbital
(Nembutal)

53
Q

Short/intermediate-acting barbiturates
are sedative - Sleep in

A

20-40 minutes lasting 5-8 hours

54
Q

Short/intermediate-acting barbiturates
are sedative - termination

A

depends on liver metabolism

55
Q

Short/intermediate-acting barbiturates
are sedative - prescribed

A

for insomnia, high abuse
potential

56
Q

Long-acting barbiturates are effective at

A

are effective for treating seizure
disorders and anxiety

57
Q

Long acting barbiturates have low

A

lipophilicity

58
Q

Long-acting barbiturates - names

A

Phenobarbital, mephobarbital

59
Q

Long-acting barbiturates - onset

A

takes 1 or more hours

60
Q

Long-acting barbiturates - metabolism

61
Q

Long-acting barbiturates lasting effects

A

10-12 hours

62
Q

Side effects and safety margin of barbiturate’s

A

Anxiolytic effects are accompanied by
cognitive side effects

63
Q
  • Anxiolytic effects of barbiturate’s are accompanied by
    cognitive side effects (3)
A
  • Mental clouding
  • Loss of judgement
  • Slowed reflexes
64
Q

barbituate Intoxication (high doses) leads to (3)

A

staggering, jumbled speech, impaired
thinking

65
Q

barbituates cause

A

Coma and death due to respiratory
depression

66
Q

REM and barbiturates

A

Alterations in REM sleep

67
Q

barbiturate’s and tolerance

A

Produce tolerance and dependence resulting in high abuse potential

68
Q

Safety margin of barbiturate’s

A

narrows due to
tolerance mechanisms

69
Q

Despite their hypnotic effects,
barbiturates do not

A

induce restful
sleep.

70
Q

sleep - Short term use results in

A

rapid sleep
onset but decreased Stage 3 & 4 sleep.

71
Q

Chronic use decreases

A

REM sleep and
stage 3 & 4 sleep and increases
spontaneous awakenings.

72
Q

Illicit use

A

High abuse potential due to rapid tolerance
and dependence

73
Q

Illicit use * Often used in conjunction with

A

amphetamines

74
Q

Often used in conjunction with
amphetamines

A

Amphetamines during the day (uppers or
pep-pills)
Barbiturates at night (downers or goofballs)

75
Q

High potential for interactions with

76
Q

Decreasing safety margin with tolerance
leads to

A

high potential for overdose

77
Q

Synaptic effects of barbiturates - Barbiturates act at the

A

GABA-A receptor

78
Q

at the
barbiturate binding site

A

Positive allosteric
modulation

79
Q

barbiturate’s and GABA affinity

A

Increases GABA affinity

80
Q

channel open time and barbituates

A

Prolongs open time

81
Q

High doses -Synaptic effects of barbiturates

A

– GABA mimetic (opens GABAA in absence of GABA)

82
Q

Barbiturate drug effects

A

Barbiturates are CNS depressants and cause
broad increases in inhibitory neurotransmission

83
Q

Barbiturate drug effects - Anticonvulsant by

A

decreasing general
excitability

84
Q

Barbiturate drug effects - Important effects in the

A

reticular formation

85
Q

Pontine

A

normally activates cortical centres

86
Q

Medullary

A

– normally supresses cortical centres

87
Q

Balance of barbiturate effect in the reticular
formation - Medullary first

A

euphoria resulting from cortical activation (disinhibitory)

88
Q

Balance of barbiturate effect in the reticular
formation - pontine first

A

relaxation, drowsiness, sleep from
cortical depression (inhibitory)

89
Q

Barbiturate abuse - Paradoxically, barbiturates decrease

A

mesolimbic DA release in the NAc through effects on VTA GABA interneurons.

90
Q

Barbiturates can be demonstrated to
reinforce through

A

microinjection into the
VTA (operant self-administration)
suggesting the same neural substrates
for addictions as other abused substances.

91
Q

Pentobarbital administration inhibits

A

NAc dopamine release and can inhibit ketamine induced dopamine release.

92
Q

Barbiturate tolerance

A

Tolerance develops through metabolic and pharmacodynamics mechanisms

93
Q

Metabolic tolerance - enzymes

A

Barbiturates induce microsomal enzymes leading to greater liver metabolism

94
Q

Metabolic tolerance: drug dose

A

Increased drug dose required to achieve same blood levels

95
Q

Metabolic tolerance - cross tolerance

A

Leads to cross-tolerance among different barbiturates

96
Q

Barbiturate tolerance Pharmacodynamic tolerance - cellular

A

Cellular changes in GABAA receptor function and expression

97
Q

Pharmacodynamic tolerance - dosage

A

Greater barbiturate dose required to elicit inhibitory effect

98
Q

Tolerance to sedative, anxiolytic and hypnotic effects are more

A

pronounced than tolerance to respiratory
depression

99
Q

intoxication induced with doses

A

4-12 times above therapeutic dose

100
Q

Peak sedative effect in

A

30-90 minutes

101
Q

Fully awake

A

4 hours after dose

102
Q

Period of cognitive impairment

A

– inarticulate speech, clouded thought,
coarse tremors of hand, depressed superficial reflexes, depression or mania

103
Q

Dependence induced by

A

increasing doses every 12 hours for 92-140 days

104
Q

Dependence trials resulted in

A

continuous mild intoxication in
most cases

105
Q

Dependence trials resulted in continuous mild intoxication in
most cases

A

Confusion, inability to perform normal tasks
* Unkempt living quarters and decreased self-care
* Irritable, aggressive, and quarrelsome
* Staggering, frequent falls and injuries

106
Q

Barbiturate withdrawal - 12-16 hours

A

12-16 hours after last dose subjects appeared to sober

107
Q

Barbiturate withdrawal - 24-36 hours

A

24-36 hours after last dose increasing anxiety and weakness developed

108
Q

24-36 hours after last dose increasing anxiety and weakness developed

A
  • At peak subjects could not stand unassisted
  • Drop in blood pressure – fainting on standing
  • Tremors, anorexia, vomiting, abdominal distress, insomnia, weight loss,
    increased startle response, hyperreflexia
109
Q

withdrawal - Significant appearance of

A

convulsions and psychosis

110
Q

Rebound hyperactivity

A

Since barbiturates enhance GABAA
function, rebound results in
hyperexcitability and convulsions

111
Q

Psychosis developed 3-5 days after
withdrawal lasting as long as

112
Q

Psychosis developed 3-5 days after
withdrawal lasting as long as 9 days

A
  • Delirium, agitation, insomnia,
    confusion, disorientation, auditory
    and visual hallucinations
  • High BP, temperature, pulse
113
Q

Withdrawal is typically managed

A

clinically

114
Q

Intermediate acting barbiturates replaced with

A

long acting drug (typically phenobarbital)

115
Q

Phenobarbital weaned

A

over a long period to
minimize severity of withdrawal

Neuro-pharmacology (26 decks)

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