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Drugs and Psychopharmacology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What happens when GABA is suppressed by alcohol?

A

the flow of chloride increases

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2
Q

What pathways are changed by alcohol?

A

AMP pathways

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3
Q

What specific neurotransmitters are more likely to be disturbed by alcohol?

A

GABA and Glutamate

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4
Q

What is a stimulant drug?

A

increases activity in your brain and nervous system. It also increases the circulation of chemicals such as cortisol and adrenaline in the body.

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5
Q

What does niacinamide adenine determine?

A

how much alcohol one can metabolize

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6
Q

_ to _ grams of alcohol can be metabolized per hour.

A

6 to 8 g

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7
Q

In what percent range would you likely have alcohol poisoning?

A

about 0.3% to 0.4%

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8
Q

Can the rate at which alcohol is metabolized be sped up?

A

no

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9
Q

Define “off label use”.

A

a drug that is not FDA approved

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10
Q

What are the 5 steps for treating alcohol dependency (pharmacotherapies)?

A
  1. reverse pharmacological effects
  2. prevent withdrawal
  3. maintenance of abstinence
  4. treat coexisting psych disorders and other related issues (depression, bipolar disorder, etc.)
  5. limit any neural-induced damage
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11
Q

What do reverse pharmacological effects mean?

A

detox

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12
Q

True or False: The use of caffeine is treated using various forms of therapy and drugs.

A

False, the use of caffeine is not treated.

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13
Q

What is the treatment of choice for treating alcohol dependency?

A

mixed approach

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14
Q

How is alcohol intervention handled (4)?

A
  1. prevent/treat some withdrawal symptoms
  2. use drugs to reduce relapse (combined with supportive therapy)
  3. treat complications
  4. reduce glutamate release and glutamate receptor regulation
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15
Q

What kind of treatment complications can come from treating alcohol dependency?

A

sleep issues and depression

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16
Q

How can glutamate receptors be regulated?

A

mood stabilizers and anticonvulsant

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17
Q

Toluene activates

A

the central reward systems in the brain

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18
Q

What did the rat study show about inhalants?

A

The rats showed an increase in stimulation in the hypothalamus as well as an increase in concentration levels. It also showed that there was an increase in depression after there was a crash in energy.

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19
Q

What are the different categories of inhalants?

A

anesthetics, solvents, office supplies (ex. white put, sharpies, etc.), gases (ex. butane lighters), household aerosol repellents (ex. hairspray, paints, cooking spray, cleaning products, etc.)

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20
Q

What age range is more likely to use and become addicted to inhalants?

A

mid-adolescents (13 to 15 million Americans)

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21
Q

Vapor is inhaled rapidly and as intoxication increases, the person becomes _.

A

disoriented

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22
Q

Why do some people die from inhalants?

A

the inhalants suppress O2

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23
Q

What is it called when a person dies from the usage of inhalants?

A

Sudden Sniffing Death Syndrome (SSDS)

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24
Q

True or False: It is not known exactly how inhalants work in the body.

A

True

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25
Q

What type of inhalant produces only light effects?

A

anesthetics

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26
Q

What is known about inhalant solvents?

A

they may slow brain activity

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27
Q

What are the effects of chronic use of inhalants?

A

damage to the liver, kidneys, parietal part of the brain, etc. chronic use can also cause dementia.

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28
Q

How is inhalant addiction treated?

A

through supportive/talk therapy

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29
Q

What are the “top two drugs of all time” according to Dr. Newell?

A

caffeine and nicotine

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30
Q

About how many Americans consume caffeine?

A

~80%

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31
Q

what are some pros to caffeine consumption?

A

mental alertness, dopaminergic effects, improvement in cognitive (when consumes in moderation) function, attention to detail, and reinforcement

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32
Q

How long does it take caffeine to reach its target?

A

~40 minutes

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33
Q

How long does the complete absorption of caffeine take?

A

~2 hours

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34
Q

Does caffeine get to the brain quickly or does it take a long time?

A

It gets to the brain fairly quickly

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35
Q

What percent of caffeine is left unchanged after it is metabolized?

A

about 10% is unchanged

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36
Q

What is the range of half-life for caffeine?

A

2 to 5 hours

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37
Q

What would cause caffeine half-life to be shortened?

A

smoking

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38
Q

What enzyme metabolizes caffeine?

A

CYP (1A2) enzyme

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39
Q

What is caffeine metabolized to?

A

paraxanthine (84%), theobromine (12%), and theophylline (4%)

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40
Q

After the __ metabolizes caffeine, the __ excrete what’s remaining into urine.

A

liver; kidneys

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41
Q

Which metabolites behave like caffeine?

A

theophylline and paraxanthine

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42
Q

Which metabolite of caffeine is inactive and can also be used to treat asthma?

A

theophylline

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43
Q

What may cause toxicity or intolerance to caffeine?

A

cross metabolism with SSRI’s

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44
Q

Caffeine stimulates the _ system.

A

nervous

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45
Q

What is a diuretic (also known as “water pills”)?

A

a drug that increases your frequency of urination to help rid your body of salt (sodium) and water

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46
Q

Caffeine is what type of drug?

A

a stimulant

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47
Q

Caffeine can be used to treat what?

A

migraines and narcolepsy

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48
Q

What are some behavioral effects of caffeine?

A

reduces fatigue, keeps you awake, alertness

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49
Q

How many cups of coffee per day is considered a heavy consumption of caffeine?

A

about 12 cups or more per day

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50
Q

How many cups of coffee per day is considered lethal? What is it called when you consume this amount or near this amount per day?

A

100 cups per day; caffeine intoxication

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51
Q

Caffeine adversely affects __ at how many milligrams?

A

muscle control; about 100 milligrams

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52
Q

What are the primary symptoms for caffeine withdraw?

A

headaches, increased agitation, and a crash

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53
Q

Caffeine exasperates _ disorder.

A

anxiety

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54
Q

Caffeinism

A

a complaint encompassing a variety of unpleasant mental and physical symptoms associated with the consumption of excessive amounts of caffeine; produces CNS and PNS stimulation

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55
Q

What are the symptoms of caffeinism?

A

restlessness, nervousness, insomnia, increased anxiety, gastrointestinal issues

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56
Q

What issues can caffeinism cause in the PNS?

A

tachycardia, hypertension, arrhythmias, GI issues

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57
Q

How does caffeine effect panic disorders?

A

symptoms are exaggerated

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58
Q

Caffeine can increase chances of getting _ disease.

A

heart

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59
Q

Caffeine can decrease flow as well as pressure in the _.

A

brain

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60
Q

Caffeine blocks which two adenosine receptors?

A

A1 and A2A

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61
Q

What happens when caffeine blocks A2A receptors?

A

the is an increase in dopamine (D2) in the frontal cortex which is where the reward effects of caffeine come from

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62
Q

Adenosine Receptors

A

neuromodulators; influence the release of neurotransmitters; exerts a depressant effect

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63
Q

What happens when adenosine receptors are blocked?

A

there will be an increase in the release of neurotransmitters in the brain; the activity of dopamine, acetylcholine, glutamate, and norepinephrine increases

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64
Q

What effects are seen when A1 is blocked by caffeine?

A

the release of dopamine and glutamate are inhibited, and sometimes acetylcholine is blocked

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65
Q

__ and __ are responsible for reward (pleasurable feeling) and the increase in alertness from caffeine.

A

dopamine and glutamate

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66
Q

__ accounts for the behavioral affects of caffeine.

A

acetylcholine

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67
Q

What is the addictive aspect of cigarettes?

A

nicotine

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68
Q

True or False: There is no medical use for nicotine.

A

True

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69
Q

In the U.S., when do most people begin smoking/become addicted to cigarettes.

A

teen years (15 to 16)

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70
Q

Most early cigarette use is related to what?

A

other drug use and psychoactive issues

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71
Q

Cigarette use in the U.S. has decreased by __ in the last 20 to 30 years.

A

half

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72
Q

What is the difference between smoking cigarettes, cigars, and pipes.

A

Cigar and pipe smoke is not inhaled like cigarette smoke

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73
Q

What is the most common way nicotine is consumed?

A

inhalation via cigarettes

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74
Q

In what way is nicotine used via patches? Why is this used?

A

Nicotine is used via patches as a slow drip. This is typically used for those who are trying to discontinue the use of cigarettes.

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75
Q

Nicotine is easily absorbed through __.

A

the lungs and skin

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76
Q

Nicotine smoke= ?

A

tar

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77
Q

Nicotine rapidly saturates the __.

A

blood

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78
Q

When nicotine leaves the lungs…

A

there isn’t as much nicotine in the blood as you’d think.

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79
Q

Cigarettes have different nicotine levels ranging from _ to _.

A

0.5 mg to 2 mg

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80
Q

~__ % of nicotine is inhaled and absorbed, the rest being absorbed by __.

A

20; CYP2A6

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81
Q

At what rate is nicotine metabolized?

A

quickly

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82
Q

What percent of nicotine is metabolized by the liver?

A

80 to 90%

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83
Q

What is the metabolite of nicotine?

A

cotinine

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84
Q

A higher level of cotinine is found in what demographic, making them more susceptible to addiction.

A

Black people

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85
Q

What is the half-life for chronic smokers?

A

~2 hours

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86
Q

What are the early symptoms of cigarette use?

A

nausea and feelings of sickness

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87
Q

Nicotine stimulates the __.

A

thalamus

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88
Q

ADH causes __.

A

fluid retention

89
Q

The antidepressant effect of nicotine makes researchers believe what?

A

smoking is self medication

90
Q

Teens are more likely to become addicted to/use cigarettes when they have a history of __.

A

ADHD and conduct disorder (rebellion of authority)

91
Q

Nicotine reduces __ and __.

A

muscle tone and weight gain

92
Q

What are the pros of nicotine?

A

-releases multiple actions in CNS which increases motor activity
-increases cognitive function
-increase in sensory motor function
-increase in attention/focus
-increase in ability to rapidly process information

93
Q

Nicotine use can lead to the increase likelihood of __.

A

panic attacks

94
Q

locus coeruleus

A

involved with physiological responses to stress and panic; behavioral arousal

95
Q

What is the result of frontal lobe activation?

A

working memory function and mood

96
Q

There is a strong connection between smoking and __.

A

adverse childhood abuse

97
Q

Nicotine activates _ which responsible for _.

A

ACH; benefits of smoking cigarettes

98
Q

Nicotinic receptors in the PNS:

A

cause an increase in blood pressure and heart rate

99
Q

Why does nicotine cause an increase in blood pressure and heart rate?

A

because epinephrine is released

100
Q

Nicotinic receptors in CNS:

A

are widely distributed throughout the brain; facilitate the release of neurotransmitters (excitatory effect)

101
Q

Mesolimbic pathway =

A

addiction pathway

102
Q

Glutamate and GABA are activated by nicotine. This has led to the debate that it may or may not produce __.

A

tolerance effects

103
Q

What are the withdrawal symptoms when smoking/nicotine use is stopped?

A

-craving for nicotine
-decrease in mood (irritation, anger, aggravation, restlessness)

104
Q

How long can nicotine/smoking withdrawal symptoms last?

A

up to a month

105
Q

Research shows that there is a(n) __ in caffeine use when people decrease or stop the use of cigarettes and/or nicotine.

A

increase

106
Q

What is the most toxic/harmful part of cigarettes?

A

tar

107
Q

There is an estimate of about __ minutes taken off of lifespan for every __ cigarette that a person smokes.

A

14; 1

108
Q

Cigarette use can lead to what type of disease (most often)?

A

cardiovascular (could also say cancer)

109
Q

Why does cigarette/nicotine use lead to cardiovascular disease?

A

Because smoking deprives the heart of less O2 and nicotine increases the amount of work that the cardiovascular system has to do

110
Q

Nicotine combined with tar can lead to…

A

heart disease, cardiovascular disease, and cancer

111
Q

Benzopyrene (Benzo[a]pyrene) (BPD)

A

major carcinogen in cigarettes

112
Q

What makes cancer more likely when smoking?

A

We all have cancer that our bodies fight off so that we do not get sick, but with the combination of nicotine and tar, the cancer suppressor gene is more suppressed. This makes cancer more likely to occur.

113
Q

What are the various treatments for nicotine addiction?

A

-“cold turkey” (doesn’t usually last long)
-psychological (relapse prevention, hasn’t worked a lot)
-acupuncture (more common in the 80s)
-replacement therapy
-pharmacotherapy approach
-replace one form of nicotine with another (cigarettes –> patches)
-a fairly successful approach
-drugs
-bupropion (antidepressant) (Zyban in cigarette treating form)
-time release capsules
-A-typical: dopamine involved
-partial nicotine receptors (agonistic)
-vaccine approach (currently in its early stages)

114
Q

Partial nicotine receptors:

A

-antagonist
-varenicline (chantics)
-increases chances of stopping smoking (up to 3x more likely)
-more successful than bupropion

115
Q

What are the side effects of partial nicotine receptors for nicotine addiction treatment?

A

nausea, GI issues, neuro-psych disturbances, increase in violence and aggression

116
Q

What form of nicotine addiction treatment is more successful than bupropion?

A

partial nicotine receptors

117
Q

What does the vaccine treatments for nicotine addiction treatment target?

A

NIC-002 and NIC-VAC

118
Q

What are the features of vaccine therapies for the treatment of nicotine addiction?

A

-has to be repeated
-intermuscular injections
-if you smoke too much it won’t work

119
Q

What is the goal of vaccine therapies for the treatment of nicotine addiction?

A

reduce antibodies and prevent bonding so the drug cannot get through the blood-brain barrier

120
Q

What will make the vaccine therapies for the treatment of nicotine addiction effective?

A

only works for smokers with high titer antibodies; only effective if you have enough antibodies

121
Q

Cocaine is a _.

A

stimulant/amphetamine

122
Q

Cocaine comes from __.

A

the leaves of the coca plant

123
Q

What are the benefits of the substances from the leaves of the coca plant?

A

increases alertness, sense of being, and indurance

124
Q

List the history of the coca plant briefly.

A

-1855: E.coca isolated
-1860: purified and used as medication
-used as an anesthetic until novocaine was discovered
-1885: no laws in the US against cocaine (was in coca-cola (18mg))
-end of 1800s: we started to recognize its issues
-1914: cocaine was made band (Harrison Act)
-for the next 15 years cocaine use decreased and was replaced with amphetamines
-1960s-1980s (more so the 80s): huge increase in the use of cocaine

125
Q

What were some causes of the skyrocketed use of cocaine in the 80s?

A

-the price of amphetamines increased
-became easier to use drugs in general
-bad time for the US (financial issues and such)
-development of crack cocaine (easy, cheap, and very accessible) (“crack baby”)

126
Q

What are the different ways that cocaine can be used?

A

smoked, snorted, or injected

127
Q

The use of cocaine was later replaced by __ in lower socioeconomic communities.

A

meth

128
Q

What is used to make meth?

A

pseudoephedrine

129
Q

Crack cocaine is insoluble in __ but highly soluble in __.

A

water; alcohol/ether

130
Q

What percent of cocaine is made up of the coca plant leaves?

A

1/2 to 1%

131
Q

How are the leaves of the coca plant prepared for cocaine?

A

they’re soaked and mashed up to make a paste and then the paste is treated with an alkaloid

132
Q

Cocaine paste contains __% of cocaine.

A

40-80% (75% likely answer for exam)

133
Q

How long does cocaine show up on blood tests and urine tests?

A

12 hours; urine: 2 weeks

134
Q

What is the most common way cocaine is administered?

A

snorting

135
Q

When snorted, what percentage of cocaine reaches the blood?

A

20-30%

136
Q

How long does it take for cocaine to reach its peak after being snorted?

A

~30 minutes

137
Q

Snorting cocaine produces what kind of effect?

A

euphoric effect (organismic effect)

138
Q

What is the time of onset for cocaine when smoked?

A

within seconds

139
Q

What percent of cocaine reaches the plasma when smoked?

A

10-30%

140
Q

When injected, cocaine __ in tissues.

A

accumulates

141
Q

What is the half-life of cocaine?

A

60 minutes

142
Q

What metabolizes cocaine?

A

Cytochrome P450 (CYP450)

143
Q

What is the metabolite of cocaine?

A

Benzoylecgonine (BE)

144
Q

What is the mechanism of action for cocaine? (3)

A
  1. potent anesthetic
  2. vasoconstrictor (constricts blood vessels)
  3. powerful reenforcing stimulant
    -this is how you become addicted
145
Q

What are the neurotransmitters that are effected by cocaine?

A

-dopamine (addictive nature)
-serotine
-norepinephrine

146
Q

What are the effects of frequent use of cocaine?

A

-increases dopamine supply in the brain leading to drug reduced psychosis (psychotic episodes, schizophrenia)
-happens quickly
-not permanent bc when stopped the person returns to normal (unless previous history of mental illness)

147
Q

How does cocaine affect dopamine, serotonin, and norepinephrine?

A

Cocaine blocks the transporters of dopamine, serotonin, and norepinephrine, causing increases in extracellular levels of these neurotransmitters.

148
Q

What is considered a low dose of cocaine?

A

25-100 mg

149
Q

What are the effects of cocaine at a low dose?

A

-hyperactivity
-rapid heartbeat
-restriction of blood vessels
-euphoria
-uncontrollable happiness
-increase in self-awareness (can be a good thing but could also be very bad)
-boastfulness
-suppression of appetite
-delays sleep (insomnia)
-decrease in mental activity

150
Q

Approximately how long do the effects of a low dose of cocaine last?

A

~30 minutes but euphoria remains for longer

151
Q

What happens after the low dose effects of cocaine wear down? what is typically done when this happens?

A

depression will set in, can lead to trimers and/or seizures (which can be deadly), sexual dysfunction, bad crash; the person will replenish and if they do not they typically have anxiety

152
Q

What happens with symptoms from cocaine as the dosage increases?

A

the symptoms will increase as well

153
Q

What can long-term use of cocaine lead to? Why?

A

increased chances of stroke, hemorrhage, and heart issues; bc it’s a stimulant and makes the body work overtime

154
Q

Increasing the dose of cocaine =

A

toxic symptoms

155
Q

What are some other symptoms of long-term cocaine use?

A

-increase in paranoia
-increase in impulse control issues
-hyperactivity

156
Q

Toxic paranoid psychosis

A

chronic paranoia and hyperactivity from cocaine use

157
Q

What is considered toxic dose of cocaine?

A

1 to 2 mg/kg

158
Q

At what point does cocaine become morbid?

A

when it is cross-linked with other drug use and/or previous psych issues

159
Q

Cocaine being used during pregnancy leads to…

A

low birth weight

160
Q

True or False: When cocaine is used during pregnancy, the baby receives more of the drug than the mother.

A

True

161
Q

What is the best approach for treating cocaine addiction?

A
  1. get the person through withdrawal
  2. treat issues that may have led to use
162
Q

True or False: There is no real consensus on how to treat cocaine use.

A

True

163
Q

What is the best way to get someone off of cocaine use?

A

treating comorbidity

164
Q

What drug can be used to help symptoms of cocaine withdrawal?

A

Ritalin

165
Q

Ritalin can restore _.

A

dopamine malfunction

166
Q

_ to _ “crack babies” are born each year.

A

50,000 to 100,000

167
Q

Pathogenic Agents

A

-sympathetic neuron system
-“mimic” agents
-epinephrine

168
Q

Amphetamines produce what kind of affects?

A

vasoconstriction
-tachycardia
-trimers
-hypertension
-increased restlessness
-increased agitation
-increased alertness

169
Q

What are the more likely symptoms of amphetamine use?

A

-increased restlessness
-increased agitation

170
Q

What was the original use of amphetamines?

A

treatment of medical issues (still used today)

171
Q

iatrogenic

A

relating to drug/amphetamine addiction caused by medical treatment (drug prescription)
-how a lot of people initially become addicted to amphetamines
-benzodiazapean
-opiates
-pain medication

172
Q

In what ways are amphetamines still used today in medicine?

A

to treat ADHD and sleep disorders (narcalepsy)

173
Q

Mechanism of Action for Amphetamines: CNS affects are a result of __.

A

newly synthesized norepinephrine and dopamine

174
Q

In the PNS, amphetamines have what effect on norepinephrine and dopamine levels?

A

Amphetamines increase norepinephrine and dopamine in the PNS

175
Q

What is the result of dopamine being released from the recumbent?

A

reward/feel good system

176
Q

What effect does amphetamine have on dopamine in the synapses? What other drug is this similar to, making it hard to tell the difference between the two?

A

dopamine is increased and reuptake is blocked; cocaine

177
Q

What form are amphetamines usually in?

A

pills

178
Q

What is considered a “low dose” of amphetamines?

A

5 to 50 mg but may differ depending on the drug

179
Q

What are some effects of low dosages of amphetamines?

A

-increased bp
-increased heart rate
-bronchial muscle relaxes
-metabolites excreated in urine almost entirely

180
Q

About how long are amphetamines detectable in urine?

A

48 hours or more

181
Q

What is considered a “moderate” dosage of amphetamines?

A

20+ mg (depends on drug)

182
Q

What are some effects of moderate dosages of amphetamines?

A

the same as low dosage effects but intensified:
-increased bp
-increased heart rate
-bronchial muscle relaxes
-metabolites excreated in urine almost entirely

183
Q

What makes higher dosages of amphetamines different from low or moderate dosages (besides the obvious)?

A

low and moderate dosages are taken orally while higher dosages are more likely to be taken intravenously

184
Q

What are some effects of moderate dosages of amphetamines?

A

-repetitious acts
-increase in violence
-increase in paranoia, anxiety, and anorexia
-psychosis (psychotic issues)
-relationship issues

185
Q

Methamphetamine is known for producing what kind of effects?

A

psychosis

186
Q

Brief history of amphetamines:

A

-1887: amphetamine first synthesized
-Early 1900s: active ingredient isolated
-1918: meth synthesized
-1920s: amphetamines used for meds
-1930s: amphetamines marked as med
-After WWII: used for fatigue and depression
-1960s: we start to see issues with addiction and abuse
-1970s: we realized the issue with amphetamines
-Today: not used as often but still used
-meth has taken over
-amphetamine abuse has increased among young people (college students)

187
Q

Why have we seen an increase in amphetamine use among young adults (college students)?

A

more pressure, ppl using it to increase performance

188
Q

Compare and contrast cocaine and amphetamines:

A

Cocaine:
-half life= 30 to 50 minutes
-snorted or smoked
-leaves system quicker which in turn makes it have faster effects
-more addictive
-metabolized more quickly

Amphetamines:
-long duration of effect (longer half-life)

Same:
-both are lipid soluble
-both have same risk for overdose
-both stored in the tissues (cross membrane readily)

189
Q

What is the “drug of choice” in today’s world?

A

methamphetamine

190
Q

About what percent of methamphetamine is manufactured at home?

A

35% or more

191
Q

Methamphetamine ingredients are readily available, what ingredient can you buy at the store? (Hint: The sale of this ingredient is banned in most states except Oklahoma)

A

pseudoephedrine

192
Q

What are the different ways methamphetamine can be used?

A

vaporized, inhaled, and smoked
-usually crystalized

193
Q

What is the half-life of methamphetamine?

A

11 hours

194
Q

Methamphetamine is excreted through the __.

A

liver and kidneys

195
Q

What percent of methamphetamine is excreted unchanged?

A

40%

196
Q

When methamphetamine is mixed with __ and __, the risk is increased as well as neurotoxicity.

A

alcohol and marijuana

197
Q

In the 1900s, methamphetamine was used to treat what?

A

ADHD

198
Q

What percent of crime is related to substance abuse?

A

60 to 70%

199
Q

Alcohol is a __ depressant.

A

CNS

200
Q

What are the general side effects of methamphetamine use?

A

-hallucinations
-increase in violence
-decrease inhibition
-more prone to infection
-heart issues

201
Q

The Thompson and Cohort study shows a link between chronic methamphetamine abuse and ___.

A

structural brain defects

202
Q

Chronic methamphetamine abuse leads to:

A

-decrease in gray matter
-increase white matter (scar replacement)
-tissue of hippocampus becomes loose (loss of memory)
-early onset alzeheimers

203
Q

The use of amphetamines during pregnancy:

A

-congenital issues
-preterm labor
-low birth rate
-increase risk of cerebral hemmoriage
-increase risk for anxiety early in age
-increase risk in ADHD

204
Q

Amphetamine tolerance:

A

-big tolerance built because of euphoric effects
-compulsive abuse
-physical dependence
-cold turkey

205
Q

What are the risks of going “cold turkey” from amphetamine?

A

severe depression and suicidal ideations

206
Q

Ice:

A

-smokable form of meth
-crystalized form of meth
-absorption is very fast

207
Q

What is the half-life for “ice”?

A

12+ hours

208
Q

What effect does Ritalin have on serotonin (5HT) and dopamine?

A

increases it

209
Q

Nonamphetamines are _ different from methamphetamine.

A

structurally

210
Q

What are some different types of nonamphetamines?

A

-ephedrine
-bath salts
-bupropion

211
Q

Flakka

A

-2nd generation synthesized
-smoked
-dopamine and norepinephrine blocker
-increases heart rate and bp
-not easily detected in urine

212
Q

ADHD is believed to be an imbalance of __.

A

serotonin and dopamine

213
Q

Ritalin is believed to balance out __.

A

dopamine and serotonin

214
Q

Nonamphetamine effects are similar to the effects of __.

A

cocaine

215
Q

Nonamphetamine balances

A

GABA and glutamate

216
Q

How is stimulant abuse treated?

A

-there are no FDA drug treatments
1. reduce withdrawal symptoms
2. reduce craving

217
Q

How is the craving for a stimulant reduced during stimulant abuse treatment?

A

-dopamine agonist is used which decreases anxiety and depression
-have to treat comorbid issues

218
Q

THP

A

decreases cocaine self-administration and chances of cocaine relapse

Drugs and Psychopharmacology (3 decks)

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