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Adv. Pharm > Quiz 3 - Sedatives & Antipsychotics > Flashcards

Quiz 3 - Sedatives & Antipsychotics Flashcards

1
Q

List the drug classes included in sedative-hypnotics

A
  • alcohol
  • inhalants of abuse
  • barbiturates
  • non-barbiturate sedative-hypnotics
  • general anesthetics
  • antiepileptic drugs
  • benzodiazepines
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2
Q

Uses of sedative-hypnotics

A
  • anxiety relief
  • insomnia
  • sedation/amnesia for procedure
  • epilepsy
  • anesthesia adjunct
  • withdrawal
  • muscle relaxation
  • diagnostic aids/psychiatry
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3
Q

Barbituric acid is a compound formed from what 2 substances? What is the other product?

A
  • formed from urea and malonic acid
  • H2O is also produced
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4
Q

2 true barbiturate agents that we may see in anesthesia

A

1) sodium thiopental
2) methohexital

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5
Q

How is the action of short-acting barbiturates terminated?

A

redistribution (Thiopental)

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6
Q

How are barbiturates metabolized?

A

Liver enzymes

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7
Q

Describe how short- and long-acting barbiturates interact with the BBB

A
  • short-acting barbiturates cross the BBB quickly
  • long-acting barbiturates are less lipid soluble and take longer to get to the brain; also produce a longer hangover
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8
Q

Oral barbiturates are (slowly/rapidly) absorbed

A

rapidly - distributed to most body tissues

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9
Q

MOA of barbiturates

A
  • modulate the effects of GABA
  • augment the opening of Cl- channels by increasing DURATION
  • results in hyperpolarization of cell membrane and makes cell membrane more resistant to neuronal excitation
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10
Q

Barbiturates (do/do not) have an antagonist.

A

do NOT

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11
Q

Barbiturate withdrawal can lead to what life-threatening event?

A

seizures

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12
Q

Tolerance to barbiturates develops more to the _____ effects and less to the ____ effects

A

More to the sedative effects and much less to the depressant effects on brainstem

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13
Q

Describe how tolerance to barbiturates develops

A
  • liver enzymes are induced more than for EtOH - up to 5x normal levels
  • up- or downregulation of neurons
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14
Q

Cross-tolerance (does/does not) occur for all sedative-hypnotics

A

DOES occur

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15
Q

Describe the physical symptoms of withdrawal from barbiturates

A
  • sleep disturbance
  • hallucinations
  • restlessness
  • disorientation
  • convulsions (life-threatening)
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16
Q

What type of medication must treatment for withdrawal from barbiturates include?

A

GABA-nergic agent

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17
Q

Describe Schedule I controlled substances and list some examples

A
  • high potential for abuse
  • no currently accepted medical use in treatment in the US
  • lack of accepted safety for use under medical supervision
  • E.g. heroin, LSD, marijuana, methaqualone
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18
Q

Describe Schedule II controlled substances and list some examples

A
  • high potential for abuse
  • currently accepted medical use in treatment in the US
  • abuse may lead to severe psychological or physical dependence
  • E.g. morphine, PCP, cocaine, methadone, methamphetamine, Fentanyl
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19
Q

Describe Schedule III controlled substances and list some examples

A
  • lower potential for abuse than Schedule I or II
  • currently accepted medical use in treatment in the US
  • abuse may lead to moderate or low physical dependence or high psychological dependence
  • E.g. anabolic steroids, codeine + Tylenol, some barbiturates
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20
Q

Describe Schedule IV controlled substances and list some examples

A
  • low potential for abuse relative to other controlled substances
  • currently accepted medical use in treatment in the US
  • abuse may lead to limited physical dependence or psychological dependence relative to other controlled substances
  • E.g. Midazolam, Valium, Xanax, Darvon, Talwin, Equanil
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21
Q

Describe Schedule V controlled substances and list some examples

A
  • low potential for abuse relative to other controlled substances
  • currently accepted medical use in treatment in the US
  • abuse may lead to limited physical dependence or psychological dependence relative to other controlled substances
  • E.g. cough medicines with codeine
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22
Q

5 problems with barbiturates

A

1) dependence
2) respiratory and CV depression
3) small TI
4) induction of microsomal enzymes
5) contraindicated in porphyria patients

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23
Q

Barbiturates have a small therapeutic index. What does this mean?

A

LD50 is not too far away from ED50

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24
Q

Benzodiazepines have largely replaced which class of drug in practice?

A

barbiturates

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25
Q

Cholral hydrate is a [drug class] primarily used with [patient population].

A

Non-barbiturate primarily used with peds

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26
Q

MOA of non-barbiturates

A
  • may work on GABA similar to barbiturates by increasing Cl- conductance
  • may work on altering membrane fluidity
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27
Q

Antagonist to non-barbiturate agents:

A

there is none

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28
Q

Describe the breakdown of chloral hydrate (Noctec)

A
  • rapidly converted by hepatic alcohol dehydrogenase to tricholoroethanol
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29
Q

Chronic use of chloral hydrate may lead to which side effects?

A
  • hepatic damage
  • severe withdrawal
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30
Q

Compound responsible for the effects of chloral hydrate:

A

tricholoroethanol

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31
Q

2 drugs that are most likely to worsen dementia in elderly patients:

A
  • anticholinergics
  • benzodiazepines
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32
Q

Barbiturates ending in “-lam” are very (hydrophilic/lipophilic). What does this mean? What are they used for?

A
  • lipophilic
  • fast on/off
  • used for panic attacks when you want a quick onset
    think of Remimazolam
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33
Q

Barbiturates ending in “-pam” are more (hydrophilic/lipophilic). What does this mean?

A
  • hydrophilic
  • slower onset
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34
Q

Cholordiazepoxide is a [drug class] more commonly known by its trade name, ______.

A
  • benzodiazepine
  • Librium
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35
Q

What structural element of Remimazolam gives it the ability for an alternative mechanism of metabolism?

A
  • ester group
  • broken down in the plasma
  • very fast on/off
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36
Q

MOA of benzodiazepines

A
  • modulate the effects of GABA
  • increase the affinity of GABA for its receptor
  • increase the FREQUENCY of Cl- channel opening
  • results in hyperpolarization of cell membranes
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37
Q

Antagonist of benzodiazepines:

A

Flumazenil

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38
Q

Uses of benzodiazepines

A
  • anxiety
  • sedative-hypnotic
  • spasticity
  • seizures
  • EtOH withdrawal
  • anesthesia

*not good analgesic

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39
Q

3 problems with benzodiazepines

A

1) dependence
2) respiratory and CV depression
3) additive/synergistic depression with other CNS depressants or EtOH

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40
Q

MOA of benzodiazepine agonist

A

facilitate GABA mediated Cl- conductance causing hyperpolarization

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41
Q

MOA of benzodiazepine antagonist

A

block the actions of benzos but NO effect on barbiturates or EtOH

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42
Q

MOA of benzodiazepine inverse agonist

A

negative modulators of GABA; produce seizures and anxiety; not used in human medicine

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43
Q

Drug that has affinity without efficacy at benzodiazepine receptors

A

Flumazenil

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44
Q

GABA-A receptor have what effect when stimulated?

A

increase Cl- conductance

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45
Q

BZ-1 receptor agonists:

A
  • Benzodiazepines
  • Zolpidem
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46
Q

BZ-1 agonists:

A

Benzodiazepines

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47
Q

GABA-B receptors have what effect when stimulated?

A
  • increase K+ conductance
  • reduction of Ca2+
  • hyperpolarization of the cell membrane
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48
Q

GABA-B receptor agonist:

A

Baclofen

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49
Q

Benzodiazepines that have active metabolites:

A
  • Chlordiazepoxide
  • Diazepam
  • Flurazepam
  • Prazepam
  • Quazepam
  • Clorazepate is metabolized to an active form in the stomach
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50
Q

How are benzodiazepines metabolized?

A

First oxidation, then glucuronide conjugation

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51
Q

3 most common benzodiazepines:

A

1) Midazolam - Versed
2) Diazepam - Valium
3) Lorazepam - Ativan

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52
Q

Benzo with the longest elimination half-time:

Why?

A

Diazepam

has an active metabolite

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53
Q

Potency of benzodiazepines D, M, L

A

L > M > D

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54
Q

Onset/peak/duration of Midazolam:

A
  • onset 1-2 min
  • peak 3-5 min
  • duration 20-60 min
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55
Q

Advantages of Midazolam:

A
  • rapid onset
  • superior amnestic
  • short DOA
  • many routes of administration
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56
Q

Disadvantages of Midazolam:

A
  • minor active metabolite
  • most resp depression
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57
Q

Onset / peak / duration of Remimazolam

A
  • onset 1-2 min
  • peak 3-5 min
  • duration 10+ min
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58
Q

Advantages of Remimazolam

A
  • rapid onset
  • short duration
  • rapid metabolism via hydrolysis by hepatic carboxylesterase-1
  • 300-fold lesser affinity for GABA-A receptors
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59
Q

Disadvantages of Remimazolam

A
  • expensive?
  • sedation lasts longer in hepatic impairment (12-16 min)
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60
Q

Onset / peak / duration of Lorazepam

A
  • onset 5-15 min
  • peak 60-90 min
  • duration 2-3 hr
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61
Q

Advantages of Lorazepam

A
  • inexpensive
  • no active metabolite
  • least amount of resp depression
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62
Q

Disadvantages of Lorazepam

A
  • much longer onset (more hydrophilic)
  • longer half-life
  • more difficult to reverse
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63
Q

Onset / peak / duration of Diazepam

A
  • onset 1-2 min
  • peak 5-7 min
  • duration 30-60 min
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64
Q

Advantages of Diazepam

A
  • inexpensive
  • rapid onset
65
Q

Disadvantages of Diazepam

A
  • many active metabolites
  • accumulates with multiple doses
  • longest half-life
  • venous irritation
66
Q

Steady state is reached after __ half-lives of a drug

A

5

67
Q

Drugs with a long half-life require a _____ to reach steady state quickly

A

bolus

68
Q

Describe how to administer benzodiazepines

A
  • loading dose
  • begin infusion at 2mg/hr
  • assess sedation
  • bolus
  • increase infusion
  • assess sedation
69
Q

Benzos and local irritation:

A

D > L > M

70
Q

Benzos and hemodynamic changes:

A

M > D > L

71
Q

Benzos and respiratory depression:

A

M > D > L

72
Q

Hemodynamic changes associated with benzodiazepines are exaggerated when…

A
  • mixed with opioids
  • hypovolemic
73
Q

Respiratory depression associated with benzodiazepines is exaggerated when…

A

mixed with opioids

74
Q

How do benzodiazepines depress central respiratory drive?

A

decreasing the ventilatory response to CO2

75
Q

MOA of Flumazenil

A

competitive inhibitor of benzodiazepine receptors

76
Q

Onset / duration of Flumazenil

A
  • onset <1 min
  • duration 45-90 min
77
Q

SE of Flumazenil

A
  • anxiety
  • tremors
  • seizures (esp with seizure hx)
78
Q

MOA of Zolpidem

A
  • non-benzodiazepine BZ-1 receptor agonist
  • increase Cl- conductance
79
Q

Advantages of Zolpidem

A
  • short DOA
  • less effect on REM sleep
  • inactive metabolites
80
Q

MOA of Suvorexant

A
  • antagonist at orexin receptors
  • blocks binding of wake-promoting neuropeptides orexin A and orexin B
  • thought to suppress wake drive
81
Q

MOA of Suvorexant

A
  • antagonist at orexin receptors
  • blocks binding of wake-promoting neuropeptides orexin A and orexin B
  • thought to suppress wake drive
82
Q

Function of the orexin neuropeptide signaling system?

Disorder associated with loss of this system?

A

central promoter of wakefulness

narcolepsy

83
Q

MOA of Busparone

A

partial agonist at 5HT1A receptors; used for anxiety

84
Q

MOA of Hydroxyzine

A

antihistamine (H1 blocker) used for anxiety

85
Q

MOA of Diphenhydramine

A

antihistamine (H1 blocker) used for sleep + anticholinergic effects

86
Q

Advantages of Etomidate

A
  • short half-life
  • little accumulation
  • little effect on HR and BP
87
Q

Disadvantage of Etomidate

A
  • myoclonus
  • adrenal suppression
88
Q

Chemistry of Propofol

A
  • alkylphenol
  • poor water soluble
89
Q

MOA of Propofol

A

stimulates a receptor that opens Cl- channels causing cell hyperpolarization

90
Q

Propofol relies on what mechanism for deactivation?

A

rapid redistribution

91
Q

Propofol has an inactive metabolite. How is it metabolized?

A

glucuronide conjugate –> CYP2B6

92
Q

Why is the length of a Propofol infusion important?

A

short infusion time = quick wake-up

long infusion time = longer wake-up

93
Q

Advantages of Propofol

A
  • short half-life
  • titratable
  • antiemetic
94
Q

Disadvantages/side effects of Propofol

A
  • hypotension
  • bradycardia
  • hyperlipidemia
  • pain on injection
  • infection source if not handled properly
  • Propofol infusion syndrome
95
Q

S/s of Propofol infusion syndrome

A
  • severe metabolic acidosis
  • rhabdomyolysis
  • renal failure
  • cardiac failure
96
Q

Propofol antagonist

A

None

97
Q

MOA of Dexmedetomidine

A

agonist at alpha-2 receptors in the locus ceruleus
a2&raquo_space;> a1

98
Q

Advantages of Dexmedetomidine

A
  • sedative
  • analgesic
  • anxiolytic
  • no resp depression
  • antishivering
  • decreased sympathetic activity
99
Q

Disadvantages of Dexmedetomidine

A
  • reduce HR
  • reduce BP
  • potentiates opioids/sedatives/anesthetics
  • dry mouth
  • vasoconstriction with rapid infusion/high doses
100
Q

Pharmacodynamics of Dexmedetomidine

A
  • highly lipid soluble
  • highly protein bound
101
Q

Relationship between A2 receptors and norepi

A

A2 receptors are part of a negative feedback system that reduces NE concentrations in the cell

102
Q

MOA of Ketamine

A
  • blocks glutamate channels
  • prevents the influx of Ca2+
  • makes cell membrane more resistant to neuronal excitation
  • produces dissociative anesthesia + analgesia
103
Q

Ketamine antagonist

A

None

104
Q

Glutamate is the primary (excitatory/inhibitory) NT in the brain

A

excitatory

105
Q

Which 2 drugs work on the NMDA glutamate receptor?

A
  • Ketamine
  • d-stereoisomer of Methadone
106
Q

Advantages of Ketamine

A
  • works on pain and sedation
  • bronchodilator
107
Q

Disadvantages of Ketamine

A
  • increased HR
  • increased BP
  • increases ICP
  • increased oral secretions
  • emergence rxns
108
Q

Which drug class can be administered with Ketamine to reduce oral secretions?

A

anticholinergic

109
Q

Serotonin plays a role in which pain pathways?

A
  • descending pain inhibitor tract
  • spinothalamic tract
110
Q

Glutamate and Substance P play a role in which pain pathway?

A

primary afferent

111
Q

Describe the biogenic amine hypothesis

A

idea of reduction of synaptic NE and serotonin as cause of depression

112
Q

Time it takes for depression medications to take effect

A

2-4 weeks

113
Q

What effect corresponds with the onset of antidepressive effects?

A

downregulation of beta receptors

AND maybe desensitizing 5HT-2 receptors

114
Q

2 chemical groups of TCAs

A

tertiary amines and secondary amines

115
Q

Chemical group of TCAs with more side effects

A

tertiary amines

116
Q

SE of TCA OD

A
  • arrhythmias
  • hypotension
  • seizures
117
Q

MOA of TCAs

A

inhibit reuptake of serotonin and norepi to treat depression

118
Q

List the 2nd generation heterocyclics

A
  • maprotaline
  • amoxapine
  • trazodone
  • buproprion
119
Q

MOA of Maprotaline

A
  • similar action as TCA but greater effect on NE than 5HT
120
Q

MOA of Amoxapine

A
  • similar action as TCA but greater effect on NE than 5HT
  • active metabolite with significant dopamine blocking activity that causes EPS
121
Q

MOA of Trazodone

A
  • serotonin reuptake inhibitor
  • 5HT-2 blocker
122
Q

MOA of Bupropion

A
  • serotonin reuptake inhibitor
  • some dopamine reuptake inhibition
  • also smoking cessation
123
Q

List the 3rd generation heterocyclics

A
  • Venlafaxine
  • Nefazodone
  • Mirtazapine
124
Q

MOA of Venlafaxine

A
  • achieves antidepressant effect by inhibiting reuptake of serotonin and NE
  • metab by P450 to an active metabolite
125
Q

MOA of Nefazodone

A

serotonin reuptake inhibitor and 5HT-2 blocker

126
Q

MOA of Mirtazapine

A

antagonizes NE and 5HT-2 and 5HT-3 receptors

127
Q

Newer TCA associated with the most seizures

A

Bupropion

128
Q

List 3 MAOIs

A
  • phenelzine
  • tranacylpromine
  • moclobemide
129
Q

MOA of MAOIs

A
  • increase concentration of NE, serotonin, and dopamine through inhibition of the MAO enzyme
130
Q

Class of antidepressants that are most clinically effective for atypical depression

A

MAOIs

131
Q

Atypical depression s/s

A
  • hypersomnia
  • hyperphagia
  • psychomotor agitation
132
Q

MAOIs interact with which food compound?

A

tyramine

133
Q

MAOIs + which drugs cause serotonin syndrome

A
  • SSRIs
  • Meperidine
134
Q

List 3 SSRIs

A
  • fluoxetine
  • paroxetine
  • sertraline
135
Q

SSRIs versus TCAs

A
  • SSRIs = efficacy, fewer SE
  • SSRIs inhibit serotonin reuptake much more than NE
136
Q

SSRIs (esp fluoxetine) is a CYP450 (inhibitor/inducer)

A

inhibitor (CYP2D6)

137
Q

Define serotonin syndrome

A
  • toxic effect d/t overstimulation of the 5HT-1A receptor in the CNS
  • usually d/t drug interaction
138
Q

Classic s/s of serotonin syndrome

A
  • agitation
  • diaphoresis
  • mydriasis
  • HTN
  • increased bowel sounds
  • hyperreflexia
  • tremor
  • clonus
139
Q

Define schizophrenia

A
  • thought disorder
  • varying presentation that may change over time
  • subdivided into types
140
Q

Describe Type 1 schizophrenia

A
  • positive signs (delusions, hallucinations, bizarre behaviors)
  • more treatable
141
Q

Describe Type 2 schizophrenia

A
  • negative signs (loss of drive, flat affect, poverty of thought and speech)
  • difficult to treat
  • manifests like depression
142
Q

Best hypothesis for schizophrenia

A
  • overactive functioning of the dopaminergic system in the limbic regions/cortex
143
Q

Which dopamine receptor is most likely target for schizophrenia drugs?

A

D2

144
Q

Stimulation of the D2 receptor causes…

A
  • inhibition of adenylyl cyclase
  • increased K+ conductance
145
Q

Describe the relationship between serotonin and dopamine in the etiology of schizophrenia

A
  • increase in serotonin relative to dopamine –> negative symptoms
  • increase in dopamine relative to serotonin –> positive symptoms
146
Q

List the second messengers of 5HT receptors

A
  • cAMP
  • K+ channels
  • IP3
  • Na-K ion channels
147
Q

Classes of drugs used to treat schizophrenia via dopamine blockade

A

1) phenothiazines (end in “-azine”)
2) thiothixene
3) butyrophenones (Haloperidol, Droperidol)

148
Q

Primary SE of phenothiazines

A

hypotension

149
Q

Primary SE of butyrophenones

A

EPS toxicity

150
Q

Describe EPS

A
  • more common with high potency neuroleptics
  • more common with parenteral routes of admin
  • occur within first 3-30 days
  • reversible upon discontinuation of drug
  • why most drugs are d/c’ed
151
Q

Mechanism of EPS

A
  • dopamine (D2) receptor blockade in motor control region of basal ganglia and substantia nigra
  • decreased dopamine
  • increased ACh
  • increased GABA
152
Q

Most common EPS

Other EPS

A
  • most common = akathisia (restlessness)
  • others = dystonia of neck/head, facial grimacing, torticollis, oculogyric crisis, bradykinesia, tremors

*dystonia is usually first to occur d/t rapid dose increase

153
Q

Treatment for early onset EPS

A

antimuscarinics (Benztopine, Trihexphenidyl)

154
Q

Describe tardive dyskinesia

A
  • latent EPS associated with long-term (2+ years) use of neuroleptic drugs
  • involuntary movements of face/lip/tongue
  • appear when drugs are stopped/reduced
  • no safe/effective tx
155
Q

Possible mechanism for TD

A

hypersensitivity of dopamine receptors in basal ganglia as a compensatory mechanism for persistent receptor blockade

156
Q

Treatment for TD

A

none

antimuscarinics worsen s/s

157
Q

Autonomic SE of antipsychotic drugs

A
  • antimuscarinic SE = decreased gastric motility, difficult urination, blurred vision, dry mouth
  • antiadrenergic SE = orthostatic hypotension, dizziness, fainting, sedation
158
Q

Endocrine SE of antipsychotic drugs

A
  • increased prolactin secretion
  • inhibited FSH, LH –> menstrual irregularities
159
Q

Relationship between dopamine and prolactin

A

dopamine inhibits prolactin secretion by acting on D2 receptors in anterior pituitary

Adv. Pharm (5 decks)

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