Part 7-1 (Psychopharmacology: sedative-hypnotics; antianxiety drugs; antidepressants) Flashcards

1
Q

Sedative-hypnotic and anti-anxiety drug Primary goals

A

Relax patient; promote normal sleep

Decrease anxiety without causing excessive sedation

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2
Q

Primary sedative-hypnotics and antianxiety drugs

A

Benzodiazepines

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3
Q

Sedative-hypnotic benzodiazepines

A

Estazolam
Quazepam
Temazepam
Triazolam

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4
Q

Antianxiety benzodiazepines

A
-Cause less sedation
Diazepam
Chlordiazepoxide
Lorazepam
Alprazolam
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5
Q

Benzodiazepines effects

A

Increases effects of GABA by binding to GABA-A receptor

More Cl- enters neuron through GABA channel

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6
Q

“Z” drugs (Sleep)

A

Zolpidem (Ambien)
Zaleplon (Sonata)
-Not benzos, but still bind to GABA receptors in different spot
-May produce fewer problems when discontinued

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7
Q

Eszopiclone (Sleep)

A

Lunesta

Not a benzo, but also binds to GABA receptors

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8
Q

Ramelteon (Sleep)

A

Rozerem

Melatonin receptor agonist

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9
Q

Azapirones (Antianxiety)

A

Buspirone
Stimulate serotonin receptors in CNS
May decrease anxiety with less sedation and dependence
Slow onset, moderate efficacy

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10
Q

Use of antidepressants as anxiolytics

A

Patients may have anxiety and depression
Antidepressents can have direct anxiolytic effects
May have fewer side effects than benzos; less addiction

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11
Q

Alternative anti-anxiety drugs

A

Quetiapine: antipsychotics
Gabapentin: antiseizure
Pregablin: antiseizure
Hydroxyzine: antihistamine

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12
Q

Sedative-hypotonic adverse effects

A

Residual effects; anterograde amnesia
Complex behaviors (Sleep walking/driving)
Rebound effect
Falls
Tolerance and dependence
Benzos may be linked to Alzheimer disease

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13
Q

Anti-anxiety drug adverse effects

A

Rebound effect (Increased anxiety when drug stopped)
Falls
Tolerance and dependence
Benzos may be linked to Alzheimer disease

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14
Q

Sleep/anti-anxiety drug rehab concerns

A

Do not treat the underlying cause

Benefits vs Sedation

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15
Q

Depression

A

Most common mental illness
Sadness that is incapacitating
Neurochemical basis

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16
Q

Depression drug strategy

A

Depression cause by defect in biogenic amines

Drugs increase or prolong the effects of one or more amine neurotransmitters

17
Q

Biogenic amines

A

Norepinephrine
Dopamine
Serotonin

18
Q

Types of antidepressants

A
  1. Selective serotonin reuptake inhibitors
  2. Serotinin norepinephrine reuptake inhibitors
  3. Tricyclics
  4. Monoamine oxydase inhibitors
  5. Others
19
Q

SSRIs

A
Fluoxetine (Prozac)
Paroxetine
Sertraline
Citalopram
Escitalopram
Fluvoxamine
20
Q

SNRIs

A

Desvenlafaxine
Duloxetine
Venlafaxine

21
Q

Tricyclics

A

Shit ton of these drugs

Named for chemical structures

22
Q

MAO inhibitors

A

Isocarboxazid
Phenelzine
Tranylcypromine

23
Q

Other antidepressents

A

Nefazodone & Trazodone: block serotonin receptors and reuptake
Bupropion: NE and dopamine reuptake inhibitor
Mirtazapine: may block presynaptic NE receptors

24
Q

Mechanisms of antidepressents

A

Prolong the effects of amine neurotransmitter by either:

a. Inhibiting reuptake of amine neurotransmitters (SSRI/SNRI/Tricyclics)
b. Decreasing neurotransmitter breakdown (MAO)

25
Q

How do increased monoamines treat depression?

A

Drugs increase activity of amine neurotransmitters
Increased NT activity increases production of brain derived neurotrophic factor
BDNF stimulates growth of neurons in hippocampus

26
Q

Tricyclics adverse effects

A
Sedation
Anticholinergic effects
Orthostatic hypotension
Arrythmias
Seizures
Fatal OD
27
Q

MAO Inhibitors adverse effects

A

CNS excitation

Increased BP

28
Q

SSRI/SNRI adverse effects

A

Generally well tolerated
May increase seizures
Some GI problems

29
Q

Serotonin Syndrome

A
Possible with all antidepressants
Occurs when CNS serotonin recepters overstimulated
Increased HR/BP
Confusion
Hallucations
Dystonias/Dyskinesias
GI problems
*Can be fatal if unchecked*
30
Q

Antidepressants off label prescribed for…

A

Chronic pain

31
Q

Antidepressant rehab concerns

A

Time lag before beneficial effects
Chance of increased depression during initial tx period
Recognize and acknowledge mood changes

32
Q

Treatment of bipolar syndome

A

Classic tx: lithium
Prevents manic episodes
Mechanisms unclear

33
Q

Lithium

A

An element that is not degraded by the liver
Have to rely on kidneys to eliminate it from body
Can accumulate rapidly

34
Q

Lithium toxicity levels

A

Maintenance phase: .6-1.2 mEq/L
Acute manic episode: 1.0-1.5 mEq/L
Toxicity begins at 1.5 mEq/L
Requires tx at >2.0 mEq/L

35
Q

Mild Lithium toxicity

A

metal taste
tremor
nausea
weak

36
Q

Moderate lithium toxicity

A
vomiting
diarrhea
more tremor
incoordinated
blurred vision
37
Q

Severe lithium toxicity

A

Confusion/hallucinations
nystagmus
dysarthria
fasciculations

38
Q

Other bipolar treatments

A

Antiseizure drugs

Antipsychotics