Exam 4 Flashcards
1
Q
What are the 3 main categories of psychedelics?
A
-Hallucinations
-Mixed stimulant-psychedelics
-Dissociative anesthetics
2
Q
Hallucinations: Primary endpoint
A
Visual hallucinations and out of body experiences - sensory distortions
3
Q
Secondary endpoint hallucinations
A
Disturbances of mood, cognition, and physiology
4
Q
What are the 5 most common hallucinogens?
A
-LSD
-Psilocybin
-Mescaline
-DMT
-NBOMe
5
Q
Lysergic acid diethylamide (LSD)
A
-most potent and notorious of the hallucinogens
-synthetic: belongs to a family of agents ergot alkaloids
6
Q
Psilocybin
A
-From hallucinogenic mushrooms
-Active metabolite is psilocin
7
Q
Mescaline
A
Found in Peyote
8
Q
Dimethyltryptamine (DMT)
A
-Found in a bunch of plants
-Can be brewed to make ayahuasca
-Small amounts can be found endogenously
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.
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
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
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
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
14
Q
LSD - Distribution
A
Only 1% goes to the brain
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
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
17
Q
LSD Physiological effects
A
-modest sympathomimetic: slight incr in HR, BP, & dilated pupils
-Slight dizziness or stomachache
-Muscle twitching or numbness
18
Q
Pseudo-Hallucinations
A
altered perceptions of things that are real - visual & auditory, time distortion, body distortion
19
Q
LSD Subjective Effects
A
-Pseudo-hallucinations
-Synesthesia
-Hypersuggestibility
-Enhanced emotionally and mood changes
20
Q
Synesthesia
A
experiencing sensory information in an incorrect sensory modality
21
Q
Hypersuggestibility
A
A state of easy influence that jeopardizes reality
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
23
Q
LSD - Dependence
A
Little psychological dependence
-No effects on the reward pathways
24
Q
LSD - Adverse effects
A
-Bad trips
-Panic reactions
-Flashbacks
-Hallucinogens Persisting Perception Disorder
25
Bad trips
sometimes called constrictive experiences
26
Panic reactions
-Altered perceptions mixing with high emotionality can lead to intense fear or sadness
-Results in pounding heart, shallow breathing, etc.
26
Hallucinogen Persisting Perception Disorder
Recurrence of certain aspects (usually unpleasant) of the drug experience (usually visual alterations) following a period of abstinence
27
Flashbacks
Short, non-distressing recurrence of a previous trip
28
Can you stop the LSD trip?
-Some effects can be blocked by administration of serotonin antagonists
-Most effects can be attenuated by an IM injection of chlorpromazine
29
MDMA - Administration
-Oral
-Absorbed in GI tract
-Peak levels after 2 hours
30
MDMA - Metabolism
-Metabolized in the liver
-Half life of 9 hrs
-Converted to MDA: an active metabolite
-SSRIs inhibit MDMA metabolism
31
MDMA - MOA
-Serotonin releaser
-inhibits serotonin uptake into storage vesicles
- reverses serotonin transporter
-Increases release of DA (like amphetamines)
-much weaker than 5-HT effects
32
MDMA - Effects
Entactogen: sense of warmth/well being
Empathogen: enhanced empathy
Desire to socialize
Mild sensory distortions, enhanced tactile sensations
Tachycardia
33
MDMA - Adverse Effects
-Neurotoxicity: drug catalog classification as potent serotonergic neurotoxin
-Multiple organ failure due to overheating and dehydration
-MDMA rebound
34
MDMA Rebound
-Occurs for 1-2 days after use
-SX include depression & lethargy while waiting to replenish DA and 5-HT
35
MDMA - Chronic Effects
-Sleep disorders
-Depression
-Anxiety
-Impulsiveness
-Memory impairment
-May persist for up to 6 months or more
36
Dissociative Anesthetics
Sedative, pain relieving drugs that produce feelings of disconnectedness from the body
-some depressant and stimulant effects
37
PCP (angel dust)
originally developed as an anesthesia
-was a good pain reliver/muscle relaxer but
didn't produce sleep
Recreational use peaked in the 1970s
38
Ketamine (special K)
-Used as an animal anesthetic
-Widespread use led to a schedule III classification in 1999
39
PCP - PK
-Administered via IV, inhalation, or insufflation
-Peak onset dependent on route (5-30 mins)
-Elimination rate is 18-51 hrs - long lasting effects
40
PCP - MOA
Serotonin - agonist
Dopamine - agonist
Glutamate - antagonist
Acetylcholine - noncompetitive antagonist at nACHR
41
PCP - Effects
Amnesia: memory impairments
Analgesia
Numbness
Hallucinations
Suspiciousness/paranoia
Aggressive behavior
Perceptual disturbances: out of body experiences
42
Mental health disorder
disorder of psychological functioning sufficiently severe to require treatment
43
Fear
negative emotion caused by real or perceived imminent danger or threat - adaptive
44
Anxiety
Worry or distress concerning potential events or outcomes - could also be adaptive
45
Anxiety Disorder
Anxiety that is not adaptive and is so severe that is disrupts everyday life - worry, hopelessness, hypertension, tachycardia
46
Specific Phobias
intense fear or anxiety related to a specific object or situation (agoraphobia)
47
Panic Disorder
-Repeated rapid onset attacks of extreme fear (panic attacks)
-Strong physiological reaction with intense apprehension, fearfulness, or terror
48
Generalized Anxiety Disorder (GAD)
-Chronic, excessive worry about events, individuals, or activities
-Continual worry and subsequent exhaustion
49
Obsessive-Compulsive Disorder (OCD)
-Distress arising from obsessions
-Compulsive behaviors attempting to reduce distress by addressing the obsessions
50
Posttraumatic Stress Disorder (PTSD)
-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
Amygdala
increased activity in response to fear, activity, and aggression
-responsible for relating stimuli with the
fearful event: fear conditioning
52
Anxiolytics drugs
-Barbiturates
-Benzodiazepines
-Z drugs: non-benzo hypnotics
-Anticonvulsants
-Antidepressants
-Buspirone
53
What are barbiturates used for?
Anti-anxiety
Sleep
Anesthesia
Anti-convulsant
54
Barbiturates - Ultra short acting
-Effects within 10-20 secs but only maintained for 30 mins
-Highly lipid soluble, stored in fats, rapidly metabolized
-Commonly abused (downers)
55
Barbiturates - Long acting
-effects felt at 1 hr to last 10-12 hrs
-poor lipid solubility and slow metabolism
56
Barbiturates - Overdose
-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
Barbiturate Abstinence Syndrome
Anxiety
Muscle weakness
Abdominal pain
Sometimes seizures following abrupt cessation of use
58
Barbiturate - MOA
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
What was the first benzodiazepine on the market?
chlordiazepoxide (Librium)
60
3 examples of benzodiazepines:
-Diazepam (Valium)
-Xanax (alprazolam)
-Klonopin (clonazepam)
61
Benzodiazepine - short acting
1-2 hours for full effect
half life 12-24 hours
prescribed for as needed anxiety
62
Benzodiazepine - intermediate or long lasting
used chronically to relieve or prevent generalized anxiety disorder, seizures, etc.
63
Benzodiazepine Withdrawal Syndrome
Depression, anxiety, mania, suicidality, and convulsions following abrupt withdrawal of chronic use: withdrawal sx, craving, & inability to reduce use are indicative of dependence
64
Benzodiazepine - MOA
positive modulator of GABA signaling
65
What are the most widely prescribed sleep aids in the world?
Z-drugs
66
Risks of Z-drugs
sleep related complex behaviors
67
What are Z-drugs?
non-benzodiazepine hypnotics
68
Anticonvulsants
-Treat seizures
-Facilitate GABA neurotransmission
69
Antidepressants
-SSRIs and SNRIs primarily
-Typically first line treatment now but not effective in over 1/3 of patients
70
Buspirone
-Partial agonist or serotonin 1a receptor
-Possibly "no abuse potential" or interaction with other depressants
71
Major depressive disorder
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
Persistent Depressive Disorder (Dysthymia)
-Depressed mood that occurs everyday for 2 yrs
-At least 2 sx listed under MDD
73
Brain Alterations
-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
Antidepressant drugs definition
Classified according to their pharmacological actions and chemical structures
75
Types of antidepressants
-MAO inhibitors
-Tricyclic antidepressants
-Selective Serotonin Reuptake Inhibitors - SSRIs
-Serotonin-Norepinephrine Reuptake Inhibitors-
SNRIs
-Atypical antidepressants
76
MAO inhibitors
Bind to MAO and prevent the breakdown of monoamines
77
MAOa
-Brain, periphery, and intestines
-Reside in dopamine and norepinephrine neurons
78
MAOb
-Primarily brain but lesser extent periphery
-Resides in serotonin and norepinephrine neurons
79
What was the first clinically used MAO inhibitor?
Iproniazid (nonselective)
80
Iproniazid
limited utility due to cheese reaction where food containing tyramine cant be broken down
81
Effects of iproniazid
Enhancement of the sympathetic NS leading to increased HR, BP, and sweating, hypertensive crisis
82
Selective MAOb inhibitors (selegilline)
concentrates effects in the brain
can be administered transdermally
-less buildup of tyramine from the intestines
83
Reversible inhibitors of MAOa (RIMA; moclobemide)
-Can be displaced when needing to break down tyramine
-Weak efficacy so not FDA approved in the US
84
Tricyclic Antidepressants definition
Inhibit the reuptake of NE and 5-HT
85
What drug category contains 3 benzene rings?
Tricyclic Antidepressants
86
SSRIs definition
Elevates 5-HT by blocing reuptake through membrane transporters
87
What was the first SSRI and why was it removed?
Zelmid and it was damaging myelin
88
What is the most commonly used SSRI?
Prozac
89
What causes serotonin syndrome at high doses?
SSRIs
90
Abrupt withdrawal of SSRI's can cause what?
Serotonin Discontinuation Syndrome
-sensory disturbances, sleeping disturbances,
flu like symptoms, GI effects, disequilibrium
91
SNRI's Definition
Enhance levels of 5-HT and NE by blocking membrane transporters
92
Examples of SNRI's:
Effexor
Cymbalta
Lyrica
93
Examples of Atypical Antidepressants
Wellbutrin
Edronax
Trintellix/Brintellix
Valdoxan/Thymanax
94
What is Bipolar Disorder?
dysfunctional fluctuations between depressive and manic mood states
95
Type I Bipolar Disorder
Severe manic episode with or without depression
96
Type II Bipolar Disorder
Less severe mania (hypomania) with depressive episodes
97
Bipolar brain alterations
-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
Mood stabilizers
drugs that reduce both depressive and manic symptoms
Ex: Lithium
99
Anticonvulsive drugs
Typically used to prevent seizures
100
Atypical antipsychotic drugs
typically used to treat schizophrenia and related disorders
101
Lithium
Lithium enters neurons through Na+ channels & participates in intracellular signaling
102
Anticonvulsant Examples
Tegretol
Valproate, Depakote
Trileptal
Lamictal
103
Anticonvulsant MOA
-Positive modulators of GABAa receptors
(enhances inhibition)
-Inhibit sodium channels (inhibits high
frequency action potentials)
104
Atypical Antipsychotic Examples
-Seroquel
-Abilify
-Zeprexa
-Risperdal
105
Example of a third generation antipsychotic
Aripiprazole (Abilify)
106
Aripiprazole (Abilify)
-Weak partial agonist for D2 receptors
-Antagonism of 5-HT2a
-Unlikely to produce EPS at therapeutic doses
-Slightly less effective than atypical antipsychotics
107
What is the purpose of antipsychotics?
Reduce positive and negative symptoms of schizophrenia while carrying a low risk of EPS
6-8 weeks to full efficacy
108
Tardive Dyskinesia
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
Extrapyramidal Side Effects of Typical Antipsychotics
tremors, muscle rigidity, involuntary movements -- similar to parkinsons disease
110
Examples of Typical Antipsychotics
Chlorpromazine & Haloperidol
111
Chlorpromazine
-Developed as an antihistamine in the 1950s
-Realized that it reduced swelling during surgery and calmed patients
112
Haloperidol
-Reduced positive symptoms of schizophrenia by antagonism at dopamine D2 receptors
-Require 6-8 weeks to full efficacy
113
The Glutamate Hypothesis
Glutamate transmission low in patients with schizophrenia
-Dopamine inhibits glutamatergic neurons in many brain areas
114
The Dopamine Hypothesis
Schizophrenia is due to excess dopamine
-treatment with antipsychotic medications should reduce dopamine
115
What is Schizophrenia?
A severe, chronic psychotic illness which results in a decline in long-term psychosocial and occupational functioning
116
Schizophrenia positive symptoms
-Delusions
-Auditory hallucinations
-Incoherent speech and thought)
-Odd behavior
117
Schizophrenia negative symptoms
-Lack of emotional expression
-Lack of motivation
-Lack of experiencing pleasure
-Reduction or lack of speech
118
Why was a black box warning placed in the packaging insert for prozac?
Because of a known increased suicide risk in children and teenagers
119
Benzodiazepines produced their effects by acting as positive modulators for ____?
GABAa receptors
120
Sedative, pain relieving drugs that produce feelings of disconnectedness from the body are known as ____?
dissociative anesthetics
121
Decreased monoaminergic activity is associated with which mental health disorder?
Depression
122
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 ______?
PTSD
123
LSD is metabolized into 2-oxo-3-hydroxy-LSD by the _____?
liver
124
The historically most-prescribed, and most well-marketed psychotherapeutic drug is ____. It is an antidepressant.
Prozac
125
A person imagining pulsing changes in the brightness of flowers printed on wallpaper is experiencing _____.
pseudo-hallucinations
126
Mental health disorders are diagnosed based on symptoms in the ____ and must be sufficiently severe enough to require treatment.
Diagnostic and Statistical Manual
