Exam 2 Flashcards
(160 cards)
1
Q
What percentage of the US uses drugs?
A
8.7%
2
Q
When was the Controlled Substances Act created and what did it establish?
A
- Established schedule of controlled substances and created the DEA.
3
Q
When was the War on Drugs and who started it?
A
1980s started by Ronald Reagan
4
Q
What defines a Schedule I controlled substance?
A
No accepted medical use, have high abuse potential (heroin, LSD, marijuana)
5
Q
What defines a Schedule II controlled substance?
A
High abuse potential with sever dependence liability (opium, morphine, codeine, cocaine)
6
Q
What defines a Schedule III controlled substance?
A
Abuse potential less than Schedules I and II, including compounds containing limited quantities of narcotics (barbiturates other than schedule II)
7
Q
What defines a Schedule IV controlled substance?
A
Substances with less addictive potential than those in Schedule III (phenobarbital, Valium, Xanax)
8
Q
What defines a Schedule V controlled substance?
A
Substances with less abusive potential than those in Schedule IV (preparations of narcotics in cough suppressants, anti-diarrheal)
9
Q
What are the three features of drug abuse and addiction?
A
Physical dependence, craving, remission/relapse
10
Q
How does the DSM define substance use disorder?
A
A maladaptive pattern of substance use for at least 12 months that has led to significant impairment or distress.
11
Q
What are examples of behavioral addiction?
A
Gambling, sex, Internet, shopping.
12
Q
What are the three phases in the cycle of drug use?
A
- Preoccupation with thoughts of using drug.
- Drug intoxication aka “bingeing”.
- Withdrawal following use with negative side effects.
13
Q
How is addiction maintained?
A
Through periods of abstinence followed by relapse.
14
Q
How does route of administration affect addiction?
A
Fast onset (IV injection, smoking) is more likely to produce addiction because of the strong euphoric effects.
15
Q
What kind of reinforcement do drugs use?
A
Most are positive reinforcers and rewarding.
16
Q
How are self-administration studies conducted?
A
Conducted with animals (and experienced human addicts) to study the effect of allowing animals to give themselves an addictive drug with a fixed-ratio.
17
Q
What motivates drug users to take the drug again?
A
Withdrawal symptoms.
18
Q
What is the motivation for “impulsive” drug use?
A
Positive reinforcement.
19
Q
What is the motivation for “compulsive” drug use?
A
Relief from withdrawal symptoms.
20
Q
How doe cues stimulate drug use?
A
Cues can cause withdrawal by activating the amygdala and anterior cingulate cortex.
21
Q
What factors amplify addiction (comorbidity)?
A
Anxiety, mood, and personality disorders.
22
Q
What pathway is important for rewarding and reinforcing the abuse of drugs?
A
The mesolimbic DA pathway.
23
Q
What are the components of a reward?
A
Feeling of pleasure, motivation, and learning/cognition.
24
Q
What is dopamine’s three roles in addiction?
A
- Release of DA produces feelings of euphoria
- Mediates incentive salience (want vs. like)
- Prediction vs. occurrence of reward
25
What neuroadaptations occur within the reward system?
Down-regulation of receptors leading to tolerance.
26
What neuroadaptations occur between the reward system and others?
Gradual recruitment of anti-reward system leading to withdrawal.
27
What brain changes occur in the brain?
Transition from nucleus accumbens to the dorsal striatum for drug-taking behavior.
28
What changes occur in the PFC in response to addiction?
Disruption of glutamate impairs ability to mediate response inhibition.
29
What is the difference of ethanol vs. methanol?
Two carbon vs. one carbon chain. Haha also methanol is toxic.
30
How is alcohol absorbed?
Easily passes from GI tract to blood and other tissues.
31
What are factors that affect alcohol absorption?
Amount of oral dose, fullness of stomach, body weight, gender.
32
How is alcohol metabolized?
In the liver ADH converts ethanol to acetaldehyde which is converted by ALDH to acetic acid which is then removed as CO2 and H20. The rest is excreted by the lungs.
33
What are the behavioral effects of alcohol?
Lowering of anxiety and inhibition, impaired memory, and reduced motor coordination.
34
What are the effects of alcohol overdose?
Unconsciousness and death.
35
How does acute alcohol tolerance work?
Drug effects are greater while BAC increases and smaller while BAC is falling.
36
How does acquired alcohol tolerance work?
Metabolic tolerance due to enzyme induction; pharmacodynamic tolerance in neurons; behavioral tolerance.
37
What are the effects of chronic alcohol use?
Increased levels of alcohol and acetaldehyde causes brain death; fatty liver; alcoholic cirrhosis.
38
How is Fetal Alcohol Syndrome caused and what are the effects?
Alcohol easily passing through placental barrier leading to developmental defects.
39
What are the specific neurochemical effects of alcohol?
Acts as NT at binding site; modifies gating mechanism of ion channels; interacts with channel protein; stimulates Gs.
40
What are the non-specific neurochemical effects of alcohol?
Disturbs relationship of protein in membrane; interacts with polar heads of phospholipids; alters lipid composition.
41
What are the effects of alcohol on GABA?
Increases GABA-mediated Cl flux; stimulates GABA release; chronically reduces GABA-mediated Cl flux.
42
What are the effects of alcohol on glutamate?
Inhibits NMDA function; reduces glutamate release; results in up-regulation of NMDA receptors.
43
What are the effects of alcohol on dopamine?
Induces DA release; chronically decreases DA release leading to withdrawal symptoms.
44
What are the effects of alcohol on endogenous opioids?
Increases endogenous opioid production; chronically reduces production leading to dysphoria seen with withdrawal.
45
How is alcoholism is characterized?
Frequency and pattern of alcohol use, more significant that total amount consumed.
46
How any drinks characterize binge drinking?
Five
47
What are the causes of alcoholism?
Genetics, personality and stress, and group attitudes towards drinking.
48
What are treatments for alcoholism?
Detoxification with benzodiazepines to prevent withdrawal coupled with psychosocial therapy.
49
What is disulfiram used for?
Treating alcoholism by causing nausea whenever alcohol is consumed.
50
What is naltrexone used for?
An opioid receptor antagonist used to treat alcoholism.
51
What is acamprosate used for?
Restores excitatory-inhibitory balance upset by alcohol; NMDA antagonist and GABAa agonist.
52
What is opium?
Derived from the poppy plant and used to create morphine.
53
What do opioids do?
Narcotic analgesic, create sense of relaxation, produce euphoria.
54
How are different opioids administrated?
Morphine: intra-muscular injection or orally; opium: smoked; heroin: snorted, subcutaneous injection, IV injection.
55
How easily are opioids absorbed?
Easily passes through BBB (more so for morphine than heroin) and easily crosses placenta.
56
How are opioids excreted?
Metabolites are excreted through urine within 24 hours.
57
What are the effects of a high opioid dose?
Elation or euphoria.
58
What are the effects of a low opioid dose?
Pain relief, drowsiness, constricted pupils.
59
What are the effects of a very high opioid dose?
Sedative effects may lead to unconsciousness, respiratory failure could lead to death.
60
What are the peripheral effects of opioids?
Used to treat diarrhea and fluid loss but causes constipation.
61
Through what method were opioid receptors discovered?
Identified by radioligand binding.
62
What are the opioid receptor subtypes?
Mu, delta, kappa, and NOP-R
63
What are endorphins?
Endogenous peptides that bind to opioid receptors.
64
What are the various types of precursor peptides?
Prodynorphin, POMC, proenkephalin, pronocieptin/orphanim FQ
65
Where are propeptides located?
Concentrated in areas related to pain modulation and mood.
66
What is the function of POMC?
Releases ACTH from the pituitary gland.
67
What is the primary opioid and function of the mu receptor?
Responds to endorphins (and morphine); modulates analgesia, feeding, and positive reinforcement.
68
What is the primary opioid and function of the delta receptor?
Responds to enkephalins and found in forebrain structures; modulate olfaction, motor integration, reinforcement, and cognitive function.
69
What is the primary opioid and function of the kappa receptor?
Responds to dynorphins and found in striatum, amygdala, hypothalamus and pituitary; regulation of pain perception, gut motility, dysphoria.
70
What is the primary opioid and function of the NOP-R receptor?
Responds to nociceptin/orphanin FQ and distributed widely in CNS and PNS; role in analgesia, feeding, learning, motor function, and neuroendocrine regulation.
71
What are the function of opioid receptors?
Metabotropic G-protein receptors that inhibit nerve activity presynaptically, postsynaptically, or axoaxonically.
72
What are the qualities of pain?
Varies in intensity and quality and the perception is highly subjective.
73
What are the two components of pain?
Fast pain that is immediate caused by fast myelinated A fibers. Slow pain is emotional and carried by slow C fibers.
74
How do opioid drugs control pain?
They mimic the inhibitory effects of endogenous opioids.
75
What areas regulate pain?
Spinal cord, periacqueductal gray, and higher brain sites.
76
How are opioids reinforced?
They lower the threshold for self stimulation and enhance the brain reward mechanism.
77
How are opioids reinforced in the brain?
Endorphins inhibit GABA cells in VTA increases DA release; dynorphin acts on kappa receptors decreasing DA release.
78
What increases opioid tolerance?
Using different opioids (cross tolerance)
79
What are the effects of opioid withdrawal?
Opioids depress CNS, thus withdrawal is rebound hyperactivity.
80
What are some commonly abused opioids?
Heroin, morphine, oxycodone, hydrocodone, methadone.
81
What is the neurobiological model of tolerance/withdrawal?
Acute administration causes reduced firing; tolerance increases firing to normal levels; withdrawal causes excess firing.
82
What are the treatment programs for opioid addiction?
Detox, use of long-acting opioids such as methadone, use of clonidine to reduce withdrawal symptoms.
83
What are the different kinds of psychostimulants?
Cocaine, amphetamines, caffeine, nicotine; causes sensorimotor activation.
84
What does cocaine come from?
Extracted alkaloid from the coca plant.
85
What are the forms of cocaine?
Cocaine freebase (smoked) and the salt cocaine HCl (orally, snorted, or IV injection)
86
What is the pharmacology of cocaine?
Easily passes through BBB leading to strong addictive properties; also rapidly eliminated.
87
What is cocaine's mechanism of action?
Blocks reuptake of DA, NE and 5-HT by binding to specific transporters at low concentrations, blocks voltage-gated Na+ channels at high concentrations (anesthetic); blocking of DAT is important for cocaine's addictive properties.
88
What are novocaine and lidocaine?
Developed from cocaine and used as local dental anesthetics .
89
What are cocaine's behavioral effects?
"High" are feelings of exhilaration and euphoria, alertness, energy, great self-confidence.
90
What is sterotypy?
Repetitive, seemingly aimless behaviors induced by higher doses of cocaine.
91
What are cocaine's physiological effects?
Cocaine is sympathomimetic (produces symptoms of sympathetic nervous system activation).
92
What mediates the cocaine reward system?
The mesolimbic DA system.
93
What does the intensity of a cocaine high depend upon?
DAT occupancy, rate of DAT occupancy (administration), and baseline DA activity in mesolimbic pathway.
94
How does cocaine addiction develop?
Starts with snorting (initial euphoria provides positive reinforcement) then switch to crack smoking, freebasing, IV injecting.
95
How does cocaine affect the PFC?
Cocaine-dependent individuals show abnormal prefrontal cortical functioning that results in poor inhibitory control
96
What causes a faster transition from recreation to compulsive use?
Animal models show that longer initial access period leads to escalated daily cocaine intake.
97
What causes cocaine tolerance?
Down-regulation of reward circuit drives increase of consumption.
98
What are the current pharmacotherapies for cocaine addiction?
There are no FDA approved medications for cocaine addiction.
99
What are the behavioral therapies for cocaine addiction?
Psychosocial treatment programs; relapse prevention therapy; contingency management program.
100
What are amphetamines?
Similar to DA in structure; first synthesized in 1887 replaced by cocaine in the '70s.
101
How are amphetamines used?
Can be taken orally, snorted, injected IV, or smoked; methanmpetamine HCl (crystal meth) is highly addictive.
102
What is the pharmacology of amphetamines?
Methamphetamines have added methyl groups, thus more potent as it is more lipid soluble and resists degradation by MAO.
103
How are amphetamines degraded?
Metabolized in the liver at a slow rate, longer high vs. cocaine.
104
What are amphetamines mechanism of action?
Inhibits VMAT increasing cytoplasmic DA levels, and reverses action of DAT increasing synaptic DA levels.
105
What are amphetamines behavioral effects?
Heightened alertness, delay in sleep onset, sustained physical effort.
106
What are amphetamines physciological effects?
Potent sympathomimetic actions by releasing NE in peripheral nervous system.
107
What are the therapeutic uses of amphetamines?
Used to treat obesity, narcolepsy, ADHD.
108
What are the effects of chronic amphetamine use?
Leads to dependence and withdrawal syndrome that takes weeks or months to subside; high-dose abuse can lead to psychotic reactions .
109
What are the neural effects of amphetamines?
Causes massive depletion of DA and damage to DA axons; also damages serotonergic fibers.
110
How is meth toxic?
Reduction in striatal DAT binding that can recover over time in abstinent addicts.
111
What is nicotine?
Alkaloid found in tobacco leaves that enters lungs via tar.
112
What is the pharmacology of nicotine?
Half-life of ~2hrs, works by activating nicotinic ACh receptors
113
How can nicotine be poisonous?
High doses lead to persistent depolarization of postsynaptic cell leading to desensitization .
114
What are nicotine's behavioral effects?
Positive mood changes and increased cognitive function.
115
What are nicotine's physiological effects?
Nicotinic receptors in VTA stimulate DA release in the nucleus accumbens; leads to acute tolerance and addiction.
116
What are the peripheral effects of nicotine?
Nicotinic receptors abundant in the PNS causing tachycardia and elevated blood pressure; also reduces appetite and increases metabolic rate.
117
What are treatments for smoking?
Nicotine replacement, bupropion (nAChR antagonist) and varenicline (reduces nicotine craving).
118
What is caffeine?
Stimulant found in coffee, tea, and cacao with a half life of four hours.
119
What are caffeine's behavioral effects?
Low doses: alertness, wakefulness, increased BP, respiration rate; high dose: caffeinism (restlessness, tachycardia, GI upset).
120
What are the effects of chronic caffeine use?
Tolerance can develop, withdrawal usually manifests as headache and fatigue but no DSM definition of caffeine addiciton.
121
What is caffeine's mechanism of action?
Antagonizes adenosine receptors in the brain.
122
What are prescription stimulants used for?
Treatment of ADHD?
123
What are common prescription stimulants?
Adderall, ritalin.
124
What is vyvanase?
Therapeutically inactive drug that becomes active after first pass metabolism in the stomach, reducing abuse potential.
125
What is hemp?
Cannabis stalk used for fibers or seeds used for oils.
126
What is marijuana?
Cannabis leaves that are smoked for recreational use.
127
What are cannabinoids?
Psychoactive compounds in cannabis.
128
What is THC?
Most prevalent cannabinoid in marijuana.
129
What is the THC content of cannabis?
Varies widely between genetic strains, growing conditions, and separating male from female plants.
130
How is marijuana consumed?
Either orally (through cookies or brownies) or smoked.
131
What are the pharmacokinetics of marijuana?
THC is easily absorbed in the lungs leading to fast rise in blood plasma levels; orally has poor absorption due to degradation in the stomach.
132
What is marijuana's mechanism of action?
Cannabinoids bind to cannabinoid receptors (CB1 in the CNS, CB2 in other tissues).
133
What are the function of cannabinoid receptors?
Metabotropic coupled to Gi leading to an inhibitory effect; often on axon terminals inhibiting the release of NT.
134
What are endocannabinoids?
Endogenous cannabinoids such as anandamide or 2-AG; act as retrograde messengers.
135
What are the research uses of cannabinoids?
Adversely affect cognitive funciton, alleviate pain, suppress vomiting, enhance food-mediated reward, adverse effects on learning and memory.
136
What are cannabinoids behavioral effects?
Buzz followed by high (euphoria), then stoned (relaxed), then come-down (tired).
137
What are cannabinoids physiological effects?
Increased blood flow to skin, heart rate, hunger.
138
What are the acute effects of cannabinoid use?
Transient psychotic symptoms, impaired cognitive function as well as psychomotor performance.
139
What reinforces cannabinoid use?
Activation of mesolimbic DA system as well as interactions with opioid systems.
140
At what age does chronic cannabis use begin?
Adolescence to young adulthood.
141
What causes cannabis tolerance?
Combination of desensitization and down-regulation of CB1 receptors.
142
What causes cannabis dependence?
Related to drug use patterns and can lead to withdrawal symptoms.
143
How is cannabis addiction treated?
Many do not become dependent but treatment usually involves cognitive-behavioral therapy
144
What are the consequences of cannabis abuse?
Decreases educational performance due to persistent cognitive deficits and lead to amotivational syndrome.
145
What are the health effects of cannabis use?
No reports of overdose but smoking can damage lungs.
146
What is the link between marijuana use and schizophrenia?
Genetic linkage between predisposition to schizophrenia and increased use of cannabis.
147
What are hallucinogens?
Cause profound subjective changes in perception of reality, thought, emotion, and consciousness (do not amplify familiar states of mind).
148
What are psychedelics?
Alter cognition and perception (LSD, mescaline).
149
What are dissociatives?
Produce analgesia and sense of detachment/dissociation (Ketamine, PCP).
150
What are deleriants?
Induce state of extreme confusion and inability to control ones actions (scopolamine, atropine).
151
What is LSD?
First synthesized from rye ergot; very powerful hallucinogenic (dose is in micrograms).
152
What are the effects of LSD?
Onset 30-90 min after ingestion, effects last 6-12 hours; vivid hallucinations, disruption of logical thought.
153
What are the different structures of hallucinogens?
Can either have serotonin-like or catecholamine-like structure.
154
What is the pharmacology of LSD?
High affinity to several 5-HT receptors (5-HT 2A and 5-HT 2C play central role in producing hallucinations).
155
What is the neural mechanism of LSD?
Activates pyramidal cells in cortical layer V which disrupts normal functioning of networks in the PFC to filter sensory information leading to hallucinations.
156
What are PCP and Ketamine?
Both first used as anesthetics and used illegally .
157
What are the effects of PCP and ketamine?
Cognitive disorganization, feeling detached from the body, drowsiness and apathy, hallucinations.
158
What is the pharmacology of PCP and ketamine?
Noncompetitive antagonists of the NMDA receptor .
159
What are the neural effects of PCP and ketamine?
Cognitive deficits from NMDA block and psychotic symptoms from increased presynaptic glutamate release.
160
How does PCP and ketamine addiction form?
Unlike LSD they are highly reinforcing and have high abuse potential by stimulating DA release (ketamine more popular due to less side effects).
