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Neuropharmacology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What percentage of the US uses drugs?

A

8.7%

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2
Q

When was the Controlled Substances Act created and what did it establish?

A
  1. Established schedule of controlled substances and created the DEA.
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3
Q

When was the War on Drugs and who started it?

A

1980s started by Ronald Reagan

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4
Q

What defines a Schedule I controlled substance?

A

No accepted medical use, have high abuse potential (heroin, LSD, marijuana)

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5
Q

What defines a Schedule II controlled substance?

A

High abuse potential with sever dependence liability (opium, morphine, codeine, cocaine)

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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)

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7
Q

What defines a Schedule IV controlled substance?

A

Substances with less addictive potential than those in Schedule III (phenobarbital, Valium, Xanax)

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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)

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9
Q

What are the three features of drug abuse and addiction?

A

Physical dependence, craving, remission/relapse

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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.

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11
Q

What are examples of behavioral addiction?

A

Gambling, sex, Internet, shopping.

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12
Q

What are the three phases in the cycle of drug use?

A
  1. Preoccupation with thoughts of using drug.
  2. Drug intoxication aka “bingeing”.
  3. Withdrawal following use with negative side effects.
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13
Q

How is addiction maintained?

A

Through periods of abstinence followed by relapse.

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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.

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15
Q

What kind of reinforcement do drugs use?

A

Most are positive reinforcers and rewarding.

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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.

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17
Q

What motivates drug users to take the drug again?

A

Withdrawal symptoms.

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18
Q

What is the motivation for “impulsive” drug use?

A

Positive reinforcement.

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19
Q

What is the motivation for “compulsive” drug use?

A

Relief from withdrawal symptoms.

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20
Q

How doe cues stimulate drug use?

A

Cues can cause withdrawal by activating the amygdala and anterior cingulate cortex.

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21
Q

What factors amplify addiction (comorbidity)?

A

Anxiety, mood, and personality disorders.

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22
Q

What pathway is important for rewarding and reinforcing the abuse of drugs?

A

The mesolimbic DA pathway.

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23
Q

What are the components of a reward?

A

Feeling of pleasure, motivation, and learning/cognition.

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24
Q

What is dopamine’s three roles in addiction?

A
  1. Release of DA produces feelings of euphoria
  2. Mediates incentive salience (want vs. like)
  3. Prediction vs. occurrence of reward
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25
Q

What neuroadaptations occur within the reward system?

A

Down-regulation of receptors leading to tolerance.

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26
Q

What neuroadaptations occur between the reward system and others?

A

Gradual recruitment of anti-reward system leading to withdrawal.

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27
Q

What brain changes occur in the brain?

A

Transition from nucleus accumbens to the dorsal striatum for drug-taking behavior.

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28
Q

What changes occur in the PFC in response to addiction?

A

Disruption of glutamate impairs ability to mediate response inhibition.

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29
Q

What is the difference of ethanol vs. methanol?

A

Two carbon vs. one carbon chain. Haha also methanol is toxic.

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30
Q

How is alcohol absorbed?

A

Easily passes from GI tract to blood and other tissues.

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31
Q

What are factors that affect alcohol absorption?

A

Amount of oral dose, fullness of stomach, body weight, gender.

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32
Q

How is alcohol metabolized?

A

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.

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33
Q

What are the behavioral effects of alcohol?

A

Lowering of anxiety and inhibition, impaired memory, and reduced motor coordination.

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34
Q

What are the effects of alcohol overdose?

A

Unconsciousness and death.

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35
Q

How does acute alcohol tolerance work?

A

Drug effects are greater while BAC increases and smaller while BAC is falling.

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36
Q

How does acquired alcohol tolerance work?

A

Metabolic tolerance due to enzyme induction; pharmacodynamic tolerance in neurons; behavioral tolerance.

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37
Q

What are the effects of chronic alcohol use?

A

Increased levels of alcohol and acetaldehyde causes brain death; fatty liver; alcoholic cirrhosis.

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38
Q

How is Fetal Alcohol Syndrome caused and what are the effects?

A

Alcohol easily passing through placental barrier leading to developmental defects.

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39
Q

What are the specific neurochemical effects of alcohol?

A

Acts as NT at binding site; modifies gating mechanism of ion channels; interacts with channel protein; stimulates Gs.

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40
Q

What are the non-specific neurochemical effects of alcohol?

A

Disturbs relationship of protein in membrane; interacts with polar heads of phospholipids; alters lipid composition.

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41
Q

What are the effects of alcohol on GABA?

A

Increases GABA-mediated Cl flux; stimulates GABA release; chronically reduces GABA-mediated Cl flux.

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42
Q

What are the effects of alcohol on glutamate?

A

Inhibits NMDA function; reduces glutamate release; results in up-regulation of NMDA receptors.

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43
Q

What are the effects of alcohol on dopamine?

A

Induces DA release; chronically decreases DA release leading to withdrawal symptoms.

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44
Q

What are the effects of alcohol on endogenous opioids?

A

Increases endogenous opioid production; chronically reduces production leading to dysphoria seen with withdrawal.

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45
Q

How is alcoholism is characterized?

A

Frequency and pattern of alcohol use, more significant that total amount consumed.

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46
Q

How any drinks characterize binge drinking?

A

Five

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47
Q

What are the causes of alcoholism?

A

Genetics, personality and stress, and group attitudes towards drinking.

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48
Q

What are treatments for alcoholism?

A

Detoxification with benzodiazepines to prevent withdrawal coupled with psychosocial therapy.

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49
Q

What is disulfiram used for?

A

Treating alcoholism by causing nausea whenever alcohol is consumed.

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50
Q

What is naltrexone used for?

A

An opioid receptor antagonist used to treat alcoholism.

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51
Q

What is acamprosate used for?

A

Restores excitatory-inhibitory balance upset by alcohol; NMDA antagonist and GABAa agonist.

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52
Q

What is opium?

A

Derived from the poppy plant and used to create morphine.

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53
Q

What do opioids do?

A

Narcotic analgesic, create sense of relaxation, produce euphoria.

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54
Q

How are different opioids administrated?

A

Morphine: intra-muscular injection or orally; opium: smoked; heroin: snorted, subcutaneous injection, IV injection.

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55
Q

How easily are opioids absorbed?

A

Easily passes through BBB (more so for morphine than heroin) and easily crosses placenta.

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56
Q

How are opioids excreted?

A

Metabolites are excreted through urine within 24 hours.

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57
Q

What are the effects of a high opioid dose?

A

Elation or euphoria.

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58
Q

What are the effects of a low opioid dose?

A

Pain relief, drowsiness, constricted pupils.

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59
Q

What are the effects of a very high opioid dose?

A

Sedative effects may lead to unconsciousness, respiratory failure could lead to death.

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60
Q

What are the peripheral effects of opioids?

A

Used to treat diarrhea and fluid loss but causes constipation.

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61
Q

Through what method were opioid receptors discovered?

A

Identified by radioligand binding.

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62
Q

What are the opioid receptor subtypes?

A

Mu, delta, kappa, and NOP-R

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63
Q

What are endorphins?

A

Endogenous peptides that bind to opioid receptors.

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64
Q

What are the various types of precursor peptides?

A

Prodynorphin, POMC, proenkephalin, pronocieptin/orphanim FQ

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65
Q

Where are propeptides located?

A

Concentrated in areas related to pain modulation and mood.

66
Q

What is the function of POMC?

A

Releases ACTH from the pituitary gland.

67
Q

What is the primary opioid and function of the mu receptor?

A

Responds to endorphins (and morphine); modulates analgesia, feeding, and positive reinforcement.

68
Q

What is the primary opioid and function of the delta receptor?

A

Responds to enkephalins and found in forebrain structures; modulate olfaction, motor integration, reinforcement, and cognitive function.

69
Q

What is the primary opioid and function of the kappa receptor?

A

Responds to dynorphins and found in striatum, amygdala, hypothalamus and pituitary; regulation of pain perception, gut motility, dysphoria.

70
Q

What is the primary opioid and function of the NOP-R receptor?

A

Responds to nociceptin/orphanin FQ and distributed widely in CNS and PNS; role in analgesia, feeding, learning, motor function, and neuroendocrine regulation.

71
Q

What are the function of opioid receptors?

A

Metabotropic G-protein receptors that inhibit nerve activity presynaptically, postsynaptically, or axoaxonically.

72
Q

What are the qualities of pain?

A

Varies in intensity and quality and the perception is highly subjective.

73
Q

What are the two components of pain?

A

Fast pain that is immediate caused by fast myelinated A fibers. Slow pain is emotional and carried by slow C fibers.

74
Q

How do opioid drugs control pain?

A

They mimic the inhibitory effects of endogenous opioids.

75
Q

What areas regulate pain?

A

Spinal cord, periacqueductal gray, and higher brain sites.

76
Q

How are opioids reinforced?

A

They lower the threshold for self stimulation and enhance the brain reward mechanism.

77
Q

How are opioids reinforced in the brain?

A

Endorphins inhibit GABA cells in VTA increases DA release; dynorphin acts on kappa receptors decreasing DA release.

78
Q

What increases opioid tolerance?

A

Using different opioids (cross tolerance)

79
Q

What are the effects of opioid withdrawal?

A

Opioids depress CNS, thus withdrawal is rebound hyperactivity.

80
Q

What are some commonly abused opioids?

A

Heroin, morphine, oxycodone, hydrocodone, methadone.

81
Q

What is the neurobiological model of tolerance/withdrawal?

A

Acute administration causes reduced firing; tolerance increases firing to normal levels; withdrawal causes excess firing.

82
Q

What are the treatment programs for opioid addiction?

A

Detox, use of long-acting opioids such as methadone, use of clonidine to reduce withdrawal symptoms.

83
Q

What are the different kinds of psychostimulants?

A

Cocaine, amphetamines, caffeine, nicotine; causes sensorimotor activation.

84
Q

What does cocaine come from?

A

Extracted alkaloid from the coca plant.

85
Q

What are the forms of cocaine?

A

Cocaine freebase (smoked) and the salt cocaine HCl (orally, snorted, or IV injection)

86
Q

What is the pharmacology of cocaine?

A

Easily passes through BBB leading to strong addictive properties; also rapidly eliminated.

87
Q

What is cocaine’s mechanism of action?

A

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
Q

What are novocaine and lidocaine?

A

Developed from cocaine and used as local dental anesthetics .

89
Q

What are cocaine’s behavioral effects?

A

“High” are feelings of exhilaration and euphoria, alertness, energy, great self-confidence.

90
Q

What is sterotypy?

A

Repetitive, seemingly aimless behaviors induced by higher doses of cocaine.

91
Q

What are cocaine’s physiological effects?

A

Cocaine is sympathomimetic (produces symptoms of sympathetic nervous system activation).

92
Q

What mediates the cocaine reward system?

A

The mesolimbic DA system.

93
Q

What does the intensity of a cocaine high depend upon?

A

DAT occupancy, rate of DAT occupancy (administration), and baseline DA activity in mesolimbic pathway.

94
Q

How does cocaine addiction develop?

A

Starts with snorting (initial euphoria provides positive reinforcement) then switch to crack smoking, freebasing, IV injecting.

95
Q

How does cocaine affect the PFC?

A

Cocaine-dependent individuals show abnormal prefrontal cortical functioning that results in poor inhibitory control

96
Q

What causes a faster transition from recreation to compulsive use?

A

Animal models show that longer initial access period leads to escalated daily cocaine intake.

97
Q

What causes cocaine tolerance?

A

Down-regulation of reward circuit drives increase of consumption.

98
Q

What are the current pharmacotherapies for cocaine addiction?

A

There are no FDA approved medications for cocaine addiction.

99
Q

What are the behavioral therapies for cocaine addiction?

A

Psychosocial treatment programs; relapse prevention therapy; contingency management program.

100
Q

What are amphetamines?

A

Similar to DA in structure; first synthesized in 1887 replaced by cocaine in the ’70s.

101
Q

How are amphetamines used?

A

Can be taken orally, snorted, injected IV, or smoked; methanmpetamine HCl (crystal meth) is highly addictive.

102
Q

What is the pharmacology of amphetamines?

A

Methamphetamines have added methyl groups, thus more potent as it is more lipid soluble and resists degradation by MAO.

103
Q

How are amphetamines degraded?

A

Metabolized in the liver at a slow rate, longer high vs. cocaine.

104
Q

What are amphetamines mechanism of action?

A

Inhibits VMAT increasing cytoplasmic DA levels, and reverses action of DAT increasing synaptic DA levels.

105
Q

What are amphetamines behavioral effects?

A

Heightened alertness, delay in sleep onset, sustained physical effort.

106
Q

What are amphetamines physciological effects?

A

Potent sympathomimetic actions by releasing NE in peripheral nervous system.

107
Q

What are the therapeutic uses of amphetamines?

A

Used to treat obesity, narcolepsy, ADHD.

108
Q

What are the effects of chronic amphetamine use?

A

Leads to dependence and withdrawal syndrome that takes weeks or months to subside; high-dose abuse can lead to psychotic reactions .

109
Q

What are the neural effects of amphetamines?

A

Causes massive depletion of DA and damage to DA axons; also damages serotonergic fibers.

110
Q

How is meth toxic?

A

Reduction in striatal DAT binding that can recover over time in abstinent addicts.

111
Q

What is nicotine?

A

Alkaloid found in tobacco leaves that enters lungs via tar.

112
Q

What is the pharmacology of nicotine?

A

Half-life of ~2hrs, works by activating nicotinic ACh receptors

113
Q

How can nicotine be poisonous?

A

High doses lead to persistent depolarization of postsynaptic cell leading to desensitization .

114
Q

What are nicotine’s behavioral effects?

A

Positive mood changes and increased cognitive function.

115
Q

What are nicotine’s physiological effects?

A

Nicotinic receptors in VTA stimulate DA release in the nucleus accumbens; leads to acute tolerance and addiction.

116
Q

What are the peripheral effects of nicotine?

A

Nicotinic receptors abundant in the PNS causing tachycardia and elevated blood pressure; also reduces appetite and increases metabolic rate.

117
Q

What are treatments for smoking?

A

Nicotine replacement, bupropion (nAChR antagonist) and varenicline (reduces nicotine craving).

118
Q

What is caffeine?

A

Stimulant found in coffee, tea, and cacao with a half life of four hours.

119
Q

What are caffeine’s behavioral effects?

A

Low doses: alertness, wakefulness, increased BP, respiration rate; high dose: caffeinism (restlessness, tachycardia, GI upset).

120
Q

What are the effects of chronic caffeine use?

A

Tolerance can develop, withdrawal usually manifests as headache and fatigue but no DSM definition of caffeine addiciton.

121
Q

What is caffeine’s mechanism of action?

A

Antagonizes adenosine receptors in the brain.

122
Q

What are prescription stimulants used for?

A

Treatment of ADHD?

123
Q

What are common prescription stimulants?

A

Adderall, ritalin.

124
Q

What is vyvanase?

A

Therapeutically inactive drug that becomes active after first pass metabolism in the stomach, reducing abuse potential.

125
Q

What is hemp?

A

Cannabis stalk used for fibers or seeds used for oils.

126
Q

What is marijuana?

A

Cannabis leaves that are smoked for recreational use.

127
Q

What are cannabinoids?

A

Psychoactive compounds in cannabis.

128
Q

What is THC?

A

Most prevalent cannabinoid in marijuana.

129
Q

What is the THC content of cannabis?

A

Varies widely between genetic strains, growing conditions, and separating male from female plants.

130
Q

How is marijuana consumed?

A

Either orally (through cookies or brownies) or smoked.

131
Q

What are the pharmacokinetics of marijuana?

A

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
Q

What is marijuana’s mechanism of action?

A

Cannabinoids bind to cannabinoid receptors (CB1 in the CNS, CB2 in other tissues).

133
Q

What are the function of cannabinoid receptors?

A

Metabotropic coupled to Gi leading to an inhibitory effect; often on axon terminals inhibiting the release of NT.

134
Q

What are endocannabinoids?

A

Endogenous cannabinoids such as anandamide or 2-AG; act as retrograde messengers.

135
Q

What are the research uses of cannabinoids?

A

Adversely affect cognitive funciton, alleviate pain, suppress vomiting, enhance food-mediated reward, adverse effects on learning and memory.

136
Q

What are cannabinoids behavioral effects?

A

Buzz followed by high (euphoria), then stoned (relaxed), then come-down (tired).

137
Q

What are cannabinoids physiological effects?

A

Increased blood flow to skin, heart rate, hunger.

138
Q

What are the acute effects of cannabinoid use?

A

Transient psychotic symptoms, impaired cognitive function as well as psychomotor performance.

139
Q

What reinforces cannabinoid use?

A

Activation of mesolimbic DA system as well as interactions with opioid systems.

140
Q

At what age does chronic cannabis use begin?

A

Adolescence to young adulthood.

141
Q

What causes cannabis tolerance?

A

Combination of desensitization and down-regulation of CB1 receptors.

142
Q

What causes cannabis dependence?

A

Related to drug use patterns and can lead to withdrawal symptoms.

143
Q

How is cannabis addiction treated?

A

Many do not become dependent but treatment usually involves cognitive-behavioral therapy

144
Q

What are the consequences of cannabis abuse?

A

Decreases educational performance due to persistent cognitive deficits and lead to amotivational syndrome.

145
Q

What are the health effects of cannabis use?

A

No reports of overdose but smoking can damage lungs.

146
Q

What is the link between marijuana use and schizophrenia?

A

Genetic linkage between predisposition to schizophrenia and increased use of cannabis.

147
Q

What are hallucinogens?

A

Cause profound subjective changes in perception of reality, thought, emotion, and consciousness (do not amplify familiar states of mind).

148
Q

What are psychedelics?

A

Alter cognition and perception (LSD, mescaline).

149
Q

What are dissociatives?

A

Produce analgesia and sense of detachment/dissociation (Ketamine, PCP).

150
Q

What are deleriants?

A

Induce state of extreme confusion and inability to control ones actions (scopolamine, atropine).

151
Q

What is LSD?

A

First synthesized from rye ergot; very powerful hallucinogenic (dose is in micrograms).

152
Q

What are the effects of LSD?

A

Onset 30-90 min after ingestion, effects last 6-12 hours; vivid hallucinations, disruption of logical thought.

153
Q

What are the different structures of hallucinogens?

A

Can either have serotonin-like or catecholamine-like structure.

154
Q

What is the pharmacology of LSD?

A

High affinity to several 5-HT receptors (5-HT 2A and 5-HT 2C play central role in producing hallucinations).

155
Q

What is the neural mechanism of LSD?

A

Activates pyramidal cells in cortical layer V which disrupts normal functioning of networks in the PFC to filter sensory information leading to hallucinations.

156
Q

What are PCP and Ketamine?

A

Both first used as anesthetics and used illegally .

157
Q

What are the effects of PCP and ketamine?

A

Cognitive disorganization, feeling detached from the body, drowsiness and apathy, hallucinations.

158
Q

What is the pharmacology of PCP and ketamine?

A

Noncompetitive antagonists of the NMDA receptor .

159
Q

What are the neural effects of PCP and ketamine?

A

Cognitive deficits from NMDA block and psychotic symptoms from increased presynaptic glutamate release.

160
Q

How does PCP and ketamine addiction form?

A

Unlike LSD they are highly reinforcing and have high abuse potential by stimulating DA release (ketamine more popular due to less side effects).

Neuropharmacology (2 decks)

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