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Psychopharmacology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

What are the 3 main categories of psychedelics?

A

-Hallucinations
-Mixed stimulant-psychedelics
-Dissociative anesthetics

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2
Q

Hallucinations: Primary endpoint

A

Visual hallucinations and out of body experiences - sensory distortions

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3
Q

Secondary endpoint hallucinations

A

Disturbances of mood, cognition, and physiology

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4
Q

What are the 5 most common hallucinogens?

A

-LSD
-Psilocybin
-Mescaline
-DMT
-NBOMe

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5
Q

Lysergic acid diethylamide (LSD)

A

-most potent and notorious of the hallucinogens
-synthetic: belongs to a family of agents ergot alkaloids

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6
Q

Psilocybin

A

-From hallucinogenic mushrooms
-Active metabolite is psilocin

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7
Q

Mescaline

A

Found in Peyote

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8
Q

Dimethyltryptamine (DMT)

A

-Found in a bunch of plants
-Can be brewed to make ayahuasca
-Small amounts can be found endogenously

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9
Q

Hallucinogens history

A

Prior to the 1960’s their use was primarily restricted to religious ceremonies as a way of communicating with the gods.

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10
Q

Albert Hofmann - Hallucinogens

A

Synthesized LSD in 1938 for the Sandoz pharmaceutical company
-experienced “inadvertent exposure” in 1943
-realized that tiny doses produce strong effects
-realized that LSD is a powerful drug

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11
Q

Timothy Leary - Hallucinogens

A

-Experimented with pure psilocybin in presence of a physician in the lab with proper controls
-Eventually resulted in his dismissal in 1963
-Started the league of spiritual discovery as his religion in 1966

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12
Q

LSD - oral administration

A

-Blotter paper, tablets, liquid LSD
-All may contain other chemicals (Amphetamine & Strychnine)
-Typical dose is 100mcg
-Most psychoactive drug known
-No overdose death ever reported

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13
Q

LSD - Absorption

A

-Effects are experienced within 30-60 mins
-Alterations in perceptions or mood at 30-40 minutes
-Full blown distortion by 1 hr

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14
Q

LSD - Distribution

A

Only 1% goes to the brain

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15
Q

LSD - Metabolism

A

-Metabolized in the liver
-Half life is ~3 hrs allowing for about 8-12 hrs of effects
-LSD and metabolites only present for ~72 hrs
-Excreted in urine and feces

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16
Q

LSD - PD

A

Acts at the serotonin receptors
-Agonist with high affinity for 5-HT 1a, 5-HT 2a, 5-HT6, & 5-HT7 receptors

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17
Q

LSD Physiological effects

A

-modest sympathomimetic: slight incr in HR, BP, & dilated pupils
-Slight dizziness or stomachache
-Muscle twitching or numbness

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18
Q

Pseudo-Hallucinations

A

altered perceptions of things that are real - visual & auditory, time distortion, body distortion

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19
Q

LSD Subjective Effects

A

-Pseudo-hallucinations
-Synesthesia
-Hypersuggestibility
-Enhanced emotionally and mood changes

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20
Q

Synesthesia

A

experiencing sensory information in an incorrect sensory modality

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21
Q

Hypersuggestibility

A

A state of easy influence that jeopardizes reality

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22
Q

LSD - Tolerance

A

-Fast and robust: no drug effect after 2-3 daily uses
-Quick recovery of effects following abstinence
-Cross tolerance occurs to other hallucinogens

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23
Q

LSD - Dependence

A

Little psychological dependence
-No effects on the reward pathways

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24
Q

LSD - Adverse effects

A

-Bad trips
-Panic reactions
-Flashbacks
-Hallucinogens Persisting Perception Disorder

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25
Q

Bad trips

A

sometimes called constrictive experiences

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26
Q

Panic reactions

A

-Altered perceptions mixing with high emotionality can lead to intense fear or sadness
-Results in pounding heart, shallow breathing, etc.

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26
Q

Hallucinogen Persisting Perception Disorder

A

Recurrence of certain aspects (usually unpleasant) of the drug experience (usually visual alterations) following a period of abstinence

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27
Q

Flashbacks

A

Short, non-distressing recurrence of a previous trip

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28
Q

Can you stop the LSD trip?

A

-Some effects can be blocked by administration of serotonin antagonists
-Most effects can be attenuated by an IM injection of chlorpromazine

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29
Q

MDMA - Administration

A

-Oral
-Absorbed in GI tract
-Peak levels after 2 hours

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30
Q

MDMA - Metabolism

A

-Metabolized in the liver
-Half life of 9 hrs
-Converted to MDA: an active metabolite
-SSRIs inhibit MDMA metabolism

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31
Q

MDMA - MOA

A

-Serotonin releaser
-inhibits serotonin uptake into storage vesicles
- reverses serotonin transporter
-Increases release of DA (like amphetamines)
-much weaker than 5-HT effects

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32
Q

MDMA - Effects

A

Entactogen: sense of warmth/well being
Empathogen: enhanced empathy
Desire to socialize
Mild sensory distortions, enhanced tactile sensations
Tachycardia

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33
Q

MDMA - Adverse Effects

A

-Neurotoxicity: drug catalog classification as potent serotonergic neurotoxin
-Multiple organ failure due to overheating and dehydration
-MDMA rebound

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34
Q

MDMA Rebound

A

-Occurs for 1-2 days after use
-SX include depression & lethargy while waiting to replenish DA and 5-HT

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35
Q

MDMA - Chronic Effects

A

-Sleep disorders
-Depression
-Anxiety
-Impulsiveness
-Memory impairment
-May persist for up to 6 months or more

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36
Q

Dissociative Anesthetics

A

Sedative, pain relieving drugs that produce feelings of disconnectedness from the body
-some depressant and stimulant effects

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37
Q

PCP (angel dust)

A

originally developed as an anesthesia
-was a good pain reliver/muscle relaxer but
didn’t produce sleep
Recreational use peaked in the 1970s

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38
Q

Ketamine (special K)

A

-Used as an animal anesthetic
-Widespread use led to a schedule III classification in 1999

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39
Q

PCP - PK

A

-Administered via IV, inhalation, or insufflation
-Peak onset dependent on route (5-30 mins)
-Elimination rate is 18-51 hrs - long lasting effects

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40
Q

PCP - MOA

A

Serotonin - agonist
Dopamine - agonist
Glutamate - antagonist
Acetylcholine - noncompetitive antagonist at nACHR

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41
Q

PCP - Effects

A

Amnesia: memory impairments
Analgesia
Numbness
Hallucinations
Suspiciousness/paranoia
Aggressive behavior
Perceptual disturbances: out of body experiences

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42
Q

Mental health disorder

A

disorder of psychological functioning sufficiently severe to require treatment

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43
Q

Fear

A

negative emotion caused by real or perceived imminent danger or threat - adaptive

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44
Q

Anxiety

A

Worry or distress concerning potential events or outcomes - could also be adaptive

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45
Q

Anxiety Disorder

A

Anxiety that is not adaptive and is so severe that is disrupts everyday life - worry, hopelessness, hypertension, tachycardia

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46
Q

Specific Phobias

A

intense fear or anxiety related to a specific object or situation (agoraphobia)

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47
Q

Panic Disorder

A

-Repeated rapid onset attacks of extreme fear (panic attacks)
-Strong physiological reaction with intense apprehension, fearfulness, or terror

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48
Q

Generalized Anxiety Disorder (GAD)

A

-Chronic, excessive worry about events, individuals, or activities
-Continual worry and subsequent exhaustion

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49
Q

Obsessive-Compulsive Disorder (OCD)

A

-Distress arising from obsessions
-Compulsive behaviors attempting to reduce distress by addressing the obsessions

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50
Q

Posttraumatic Stress Disorder (PTSD)

A

-Persistent state of physiological arousal or an exaggerated response to certain stimuli (associated with the traumatic event)
-Great fear, feelings of helplessness, or even horror concerning the causative event

51
Q

Amygdala

A

increased activity in response to fear, activity, and aggression
-responsible for relating stimuli with the
fearful event: fear conditioning

52
Q

Anxiolytics drugs

A

-Barbiturates
-Benzodiazepines
-Z drugs: non-benzo hypnotics
-Anticonvulsants
-Antidepressants
-Buspirone

53
Q

What are barbiturates used for?

A

Anti-anxiety
Sleep
Anesthesia
Anti-convulsant

54
Q

Barbiturates - Ultra short acting

A

-Effects within 10-20 secs but only maintained for 30 mins
-Highly lipid soluble, stored in fats, rapidly metabolized
-Commonly abused (downers)

55
Q

Barbiturates - Long acting

A

-effects felt at 1 hr to last 10-12 hrs
-poor lipid solubility and slow metabolism

56
Q

Barbiturates - Overdose

A

-Risk of accidental overdose is high
-Deaths occur from respiratory depression
-Tolerance develops to the therapeutic effects, but not the respiratory depressant effects
-If combined with alcohol, asphyxiation can occur

57
Q

Barbiturate Abstinence Syndrome

A

Anxiety
Muscle weakness
Abdominal pain
Sometimes seizures following abrupt cessation of use

58
Q

Barbiturate - MOA

A

Positive modulator of GABAa signaling
-barbiturate site on the GABAa receptor
-anxiolytic effects come from inhibition of
amygdala function
-respiratory depression due to effects on the
medulla

59
Q

What was the first benzodiazepine on the market?

A

chlordiazepoxide (Librium)

60
Q

3 examples of benzodiazepines:

A

-Diazepam (Valium)
-Xanax (alprazolam)
-Klonopin (clonazepam)

61
Q

Benzodiazepine - short acting

A

1-2 hours for full effect
half life 12-24 hours
prescribed for as needed anxiety

62
Q

Benzodiazepine - intermediate or long lasting

A

used chronically to relieve or prevent generalized anxiety disorder, seizures, etc.

63
Q

Benzodiazepine Withdrawal Syndrome

A

Depression, anxiety, mania, suicidality, and convulsions following abrupt withdrawal of chronic use: withdrawal sx, craving, & inability to reduce use are indicative of dependence

64
Q

Benzodiazepine - MOA

A

positive modulator of GABA signaling

65
Q

What are the most widely prescribed sleep aids in the world?

A

Z-drugs

66
Q

Risks of Z-drugs

A

sleep related complex behaviors

67
Q

What are Z-drugs?

A

non-benzodiazepine hypnotics

68
Q

Anticonvulsants

A

-Treat seizures
-Facilitate GABA neurotransmission

69
Q

Antidepressants

A

-SSRIs and SNRIs primarily
-Typically first line treatment now but not effective in over 1/3 of patients

70
Q

Buspirone

A

-Partial agonist or serotonin 1a receptor
-Possibly “no abuse potential” or interaction with other depressants

71
Q

Major depressive disorder

A

At least 5 symptoms within a 2 week period
-depressed mood
-fatigue
-feeling worthless
-thoughts of suicide
-change in body weight
-lack of pleasure

72
Q

Persistent Depressive Disorder (Dysthymia)

A

-Depressed mood that occurs everyday for 2 yrs
-At least 2 sx listed under MDD

73
Q

Brain Alterations

A

-Overactive amygdala
-Volume reductions in the hippocampus
-Decreased energy metabolism & volume
reductions in the prefrontal cortex
-Volume reductions and underactivity in the nucleus accumbens/basal ganglia

74
Q

Antidepressant drugs definition

A

Classified according to their pharmacological actions and chemical structures

75
Q

Types of antidepressants

A

-MAO inhibitors
-Tricyclic antidepressants
-Selective Serotonin Reuptake Inhibitors - SSRIs
-Serotonin-Norepinephrine Reuptake Inhibitors-
SNRIs
-Atypical antidepressants

76
Q

MAO inhibitors

A

Bind to MAO and prevent the breakdown of monoamines

77
Q

MAOa

A

-Brain, periphery, and intestines
-Reside in dopamine and norepinephrine neurons

78
Q

MAOb

A

-Primarily brain but lesser extent periphery
-Resides in serotonin and norepinephrine neurons

79
Q

What was the first clinically used MAO inhibitor?

A

Iproniazid (nonselective)

80
Q

Iproniazid

A

limited utility due to cheese reaction where food containing tyramine cant be broken down

81
Q

Effects of iproniazid

A

Enhancement of the sympathetic NS leading to increased HR, BP, and sweating, hypertensive crisis

82
Q

Selective MAOb inhibitors (selegilline)

A

concentrates effects in the brain
can be administered transdermally
-less buildup of tyramine from the intestines

83
Q

Reversible inhibitors of MAOa (RIMA; moclobemide)

A

-Can be displaced when needing to break down tyramine
-Weak efficacy so not FDA approved in the US

84
Q

Tricyclic Antidepressants definition

A

Inhibit the reuptake of NE and 5-HT

85
Q

What drug category contains 3 benzene rings?

A

Tricyclic Antidepressants

86
Q

SSRIs definition

A

Elevates 5-HT by blocing reuptake through membrane transporters

87
Q

What was the first SSRI and why was it removed?

A

Zelmid and it was damaging myelin

88
Q

What is the most commonly used SSRI?

A

Prozac

89
Q

What causes serotonin syndrome at high doses?

A

SSRIs

90
Q

Abrupt withdrawal of SSRI’s can cause what?

A

Serotonin Discontinuation Syndrome
-sensory disturbances, sleeping disturbances,
flu like symptoms, GI effects, disequilibrium

91
Q

SNRI’s Definition

A

Enhance levels of 5-HT and NE by blocking membrane transporters

92
Q

Examples of SNRI’s:

A

Effexor
Cymbalta
Lyrica

93
Q

Examples of Atypical Antidepressants

A

Wellbutrin
Edronax
Trintellix/Brintellix
Valdoxan/Thymanax

94
Q

What is Bipolar Disorder?

A

dysfunctional fluctuations between depressive and manic mood states

95
Q

Type I Bipolar Disorder

A

Severe manic episode with or without depression

96
Q

Type II Bipolar Disorder

A

Less severe mania (hypomania) with depressive episodes

97
Q

Bipolar brain alterations

A

-Reduced activity in frontal and temporal lobes of RIGHT hemisphere associated with MANIC episodes

-Reduced activity in frontal and temperal lobes of LEFT hemisphere associated with DEPRESSIVE episodes

-Enlarged basal ganglia & thalamus
-Excessive activity in cortical white matter areas for unknown causes

98
Q

Mood stabilizers

A

drugs that reduce both depressive and manic symptoms
Ex: Lithium

99
Q

Anticonvulsive drugs

A

Typically used to prevent seizures

100
Q

Atypical antipsychotic drugs

A

typically used to treat schizophrenia and related disorders

101
Q

Lithium

A

Lithium enters neurons through Na+ channels & participates in intracellular signaling

102
Q

Anticonvulsant Examples

A

Tegretol
Valproate, Depakote
Trileptal
Lamictal

103
Q

Anticonvulsant MOA

A

-Positive modulators of GABAa receptors
(enhances inhibition)
-Inhibit sodium channels (inhibits high
frequency action potentials)

104
Q

Atypical Antipsychotic Examples

A

-Seroquel
-Abilify
-Zeprexa
-Risperdal

105
Q

Example of a third generation antipsychotic

A

Aripiprazole (Abilify)

106
Q

Aripiprazole (Abilify)

A

-Weak partial agonist for D2 receptors
-Antagonism of 5-HT2a
-Unlikely to produce EPS at therapeutic doses
-Slightly less effective than atypical antipsychotics

107
Q

What is the purpose of antipsychotics?

A

Reduce positive and negative symptoms of schizophrenia while carrying a low risk of EPS
6-8 weeks to full efficacy

108
Q

Tardive Dyskinesia

A

motor disorder with primary sx include involuntary smacking & sucking movements of the lips, thrusting and rolling of the tongue, lateral jaw movements, and puffing of the cheeks

109
Q

Extrapyramidal Side Effects of Typical Antipsychotics

A

tremors, muscle rigidity, involuntary movements – similar to parkinsons disease

110
Q

Examples of Typical Antipsychotics

A

Chlorpromazine & Haloperidol

111
Q

Chlorpromazine

A

-Developed as an antihistamine in the 1950s
-Realized that it reduced swelling during surgery and calmed patients

112
Q

Haloperidol

A

-Reduced positive symptoms of schizophrenia by antagonism at dopamine D2 receptors
-Require 6-8 weeks to full efficacy

113
Q

The Glutamate Hypothesis

A

Glutamate transmission low in patients with schizophrenia
-Dopamine inhibits glutamatergic neurons in many brain areas

114
Q

The Dopamine Hypothesis

A

Schizophrenia is due to excess dopamine
-treatment with antipsychotic medications should reduce dopamine

115
Q

What is Schizophrenia?

A

A severe, chronic psychotic illness which results in a decline in long-term psychosocial and occupational functioning

116
Q

Schizophrenia positive symptoms

A

-Delusions
-Auditory hallucinations
-Incoherent speech and thought)
-Odd behavior

117
Q

Schizophrenia negative symptoms

A

-Lack of emotional expression
-Lack of motivation
-Lack of experiencing pleasure
-Reduction or lack of speech

118
Q

Why was a black box warning placed in the packaging insert for prozac?

A

Because of a known increased suicide risk in children and teenagers

119
Q

Benzodiazepines produced their effects by acting as positive modulators for ____?

A

GABAa receptors

120
Q

Sedative, pain relieving drugs that produce feelings of disconnectedness from the body are known as ____?

A

dissociative anesthetics

121
Q

Decreased monoaminergic activity is associated with which mental health disorder?

A

Depression

122
Q

The disorder characterized by a persistent state of physiological arousal or an exaggerated response to certain stimuli (associated with the traumatic event) is known as ______?

A

PTSD

123
Q

LSD is metabolized into 2-oxo-3-hydroxy-LSD by the _____?

A

liver

124
Q

The historically most-prescribed, and most well-marketed psychotherapeutic drug is ____. It is an antidepressant.

A

Prozac

125
Q

A person imagining pulsing changes in the brightness of flowers printed on wallpaper is experiencing _____.

A

pseudo-hallucinations

126
Q

Mental health disorders are diagnosed based on symptoms in the ____ and must be sufficiently severe enough to require treatment.

A

Diagnostic and Statistical Manual

Psychopharmacology (1 decks)

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