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345A > Stimulants > Flashcards

Stimulants Flashcards

1
Q

…-containing sodas first appeared in 1885 with the introduction of Coca-Cola.

A

Caffeine

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2
Q

Today, more than ..% of sodas on the market contain caffeine, most of which is synthetically manufactured.

A

60

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3
Q

how much can does the GRAS say is safe

A

.02=71mg per can

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4
Q

how did energy drinks get around the caffeine restrictions

A

marketing caffeinated drinks as dietary supplements, rather than as food products, to circumvent regulations on caffeine content.

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5
Q

energy drinks have less caffeine than a cup coffee

A

yes but contain other stimulating ingredients likely not included in the caffeine count. not on label

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6
Q

Energy drinks may also contain: …, such as taurine, tyrosine, L-carnitine, L-tryptophan, L-arginine, and L-theanine; vitamins, including A, B, C, and E; minerals, such as iron or calcium

A

amino acids

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7
Q

Canada, energy drinks are regulated by Health Canada whose guidelines state that a single-serving container have no more than … caffine

A

180mg

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8
Q

men consume more coffins

A

t

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9
Q

Nutrition Examination Surveys showed that approxi-mately ..`% of children and adolescents aged 6–18 years consume caffeine.

A

75

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10
Q

nowadays where are kids getting caffeine from

A

soda
tea
coffee
energy drinks

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11
Q

when given for medical reasons, the purified drugs sometimes cause nausea and gastric irri-tation, especially in children. In such cases, the drugs may be given in the form of a …3

A

rectal suppository or by intramus-cular or intravenous routes

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12
Q

what is coffin used for transdermally

A

anti-cellulite and anti-aging cosmetics and creams

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13
Q

The methylxanthines are bases; how would you expect this to effect absorption

A

when they are dissolved in the acidic environment of the digestive tract, you might expect them to be highly ionized and, therefore, not lipid soluble (but very low Kpa= won’t ionize

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14
Q

how easily are they absorbed

A

all of it is absorbed and quickly through stomach and small intestine

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15
Q

how long after cup of coffee for peak blood levels

A

cleared from stomach in 20min peak blood levels 45 to 75min

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16
Q

The caffeine in coffee, tea, energy drinks, and choco-late exists and is consumed in its … form. and …. for medical purposes

A

alkaloid, salts

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17
Q

ask her about page 202

A

…

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18
Q

does caffeine go through entire body

A

throughout the body’s tissues and reaches all organs, although the rates of entering and leaving the organs may vary

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19
Q

About 10 to 30% of caffeine in the blood becomes bound to protein and trapped in the …

A

circu-latory system

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20
Q

how easily does cat pass blood brain and placental barrier

A

super easy

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21
Q

what is Theophylline used for

A

respiratory disorders

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22
Q

what is theobromine used for

A

chocolate

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23
Q

Theophylline and theobromine are slower to pass through the blood–brain barrier. why

A

are less lipid soluble than caffeine

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24
Q

how do we get rid of caffeine

A

1% in urine

The remaining 99% is metabolized almost exclu-sively in the liver

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25
Q

what enzyme in liver breaks down caffeine

A

cytochrome P450 superfamily enzyme: CYP1A2

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26
Q

within vs between individuals how does the half life of caffeine breakdown differ

A

consistent in individual

differ between average 5 hours to excrete all metabolites

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27
Q

There is evidence that caffeine’s half-life may be …

A

dose-dependent (faster with lower dose= constant rate )

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28
Q

The addition of …which itself contains 4–8% caffeine by weight, may prolong the half-life of caffeine

A

guaraná,

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29
Q

a number of factors affect the rate of caffeine metabo-lism and elimination from the body

A

genes

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30
Q

how do genes influence

A

The CYP1A2 gene carries instructions for building the caffeine-metabolizing cyto-chrome P450 enzyme. Individuals who express the CYP1A2*1A gene form are rapid caffeine metabolizers while those who carry the

CYP1A2*1F gene form are slow caffeine metabolizers = more effects

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31
Q

caf-feine metabolism is slowed by alcohol and grapefruit juice but speeded by broccoli, and smokers eliminate caffeine nearly twice as quickly as nonsmokers, slowed with antibiotics: why does this happen

A

The CYP1A2 enzyme can also be stimulated or inhib-ited by various foods and medications

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32
Q

how does caffeine digestion differ in females

A

hormones; longer half life after ovulation
contraceptives= longer half life
less elimination when pregnant

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33
Q

how does caffeine digestion differ in females

A

hormones; longer half life after ovulation
contraceptives= longer half life
less elimination when pregnancy increases half life

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34
Q

how much can do babies excrete

A

due to immaturity of the liver’s CYP1A2 enzyme system, and they excrete about 85% of caffeine unchanged in urine.= 100 hours

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35
Q

An adult-like pattern of caffeine metabolism and excretion does not develop until what age

A

about 7 to 9 months of age

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36
Q

how does half life differ in nonhuman species

A

Dif metabolism

Dif enzymes and metabolites

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37
Q

The effects of the methylxanthines on neural functioning arise from their structural similarity to the neurotransmitter …

A

adenosine.

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38
Q

how does caffeine interact with adenosine

A

is an adenosine receptor blocker (A1 and A2 receptor subtypes

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39
Q

where are A1 receptors in the brain

A

A1 receptors are distributed widely throughout the brain with the highest densities found in the hippocampus, cerebellum, cerebral cortex, and certain thalamic nuclei. Moderate densities are found in the sub-stantia nigra, neostriatum, ventral tegmental area, and nucleus accumbens

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40
Q

where are adenosine receptors

A

post and presynaptic

heteroreceptor

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41
Q

what NT is A1 inhibiting (6)

A

inhibit neurotransmitter release from neurons producing acetylcholine, GABA, glu-tamate, norepinephrine, serotonin, and dopamine

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42
Q

Caffeine is an adenosine receptor blocker, exerting its effects mainly at …2…receptor subtypes.

A

A1 and A2A

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43
Q

where are A2 receptors located

A

concen-trated in dopamine-rich regions of the brain, primarily the dorsal striatum and nucleus accumbens

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44
Q

is the rewarding effect of caffeine due to a direct or indirect effect

A

both

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45
Q

what does a low and high level of adenosine subjectively feel like

A 
high= sleepy 
low= alert
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46
Q

when is caffeine most effective

A

when adenosine levels are high

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47
Q

what NTs do caffeine effect indirectly

A 
Ach = increases fight or flight 
block inhibitory effects of glutamate
more nonep
other monomines (5HT and DA)
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48
Q

why can lots of caffeine cause siesires

A

Blockade of adenos-ine’s inhibitory effects on glutamate neurons helps explain why high doses of caffeine can lead to seizures.

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49
Q

what explains coffins psychomotor and reinforcing effects

A

dopamine

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50
Q

how does caffeine increase dopamine

A

blocks A1 receptors located on dopamine terminals = more release of dopamine

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51
Q

what is a heteroreceptor

A

a receptor regulating the synthesis and/or the release of mediators other than its own ligand.

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52
Q

what are receptor mosaics

A

two or more receptors are attached to each other and consequently influence one another’s operation

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53
Q

what does caffeine have to do with receptor masaics

A

The operation of receptor mosaics com-prised of adenosine and dopamine (A1–D1 and A2A–D2) receptors is impacted by caffeine so that dopamine neuro-transmission is enhanced in the striatum

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54
Q

what happens when you combine alc with caffeine

A

alc increased adenosine by enhancing Neurotransmission

caf antagonizes aden receptors= feel less drunk and more alert

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55
Q

why do alc beverages with caffeine increase desire to drink those beverages

A

Like caffeine, alcohol enhances dopamine neurotransmission. The joint actions of caffeine and alco-hol on dopamine activity= reinforcement

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56
Q

what does it mean to say can has discriminitive stimulus properties

A

stimulus that has stimulus control over behavior because the behavior was reliably reinforced in the presence of that stimulus in the past.

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57
Q

what does psychomotor stimulants mean

A

stim CNS through brain chemical

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58
Q

The methylxanthines stimulate the release of… from the adrenal glands and increase sympathetic nervous system activity, with accompanying physiological changes in …3

A

epinephrine

vascular tone, heart rate, and body temperature

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59
Q

caffeine increase blood pressure

A

t but only in newbies

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60
Q

what is tachycar-dia

A

condition that makes your heart beat more than 100 times per minute (only from high dose consumption in nonaccustom ppl)

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61
Q

At doses of 5 to 10 cups of coffee per day, caffeine can cause ….

A

sensory distur-bances, such as ringing in the ears and seeing flashes of light, as well as mild delirium and excitement.

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62
Q

The regula-tory centers of the … are also stimulated by high doses of caffeine, producing an increase in the rate and depth of breathing.

A

medulla (used for babies born with breathing problems)

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63
Q

what does caffeine do outside the CNS

A

direct actions on the muscles: smooth (involuntary) mus-cles tend to relax, and striated (voluntary) muscles increase in strength

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64
Q

theophylline: Smooth muscle relaxation results in …

A

dilation of the bronchi of the lungs and a decrease in airway resistance

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65
Q

which blood vessels does cad dilate which does it constrict

A

dilate: endothelial cells (those that line arterial walls),

constrict in brain

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66
Q

Adenosine-receptor binding can produces vasodilation or vasoconstriction?`

A

either , depending on the target organ and the type of receptor activated.

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67
Q

At moderate doses (~250 mg), caffeine produces … and can reduce cerebral blood flow by as much as 30%

A

vasoconstriction

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68
Q

what does caffeine do the headaches

A

Because dilation of cerebral blood vessels is associated

with headache, caffeine administration can alleviate head-ache pain and is added to many over-the-counter analgesics.

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69
Q

which coffee drinkers have the most headaches

A

low
moderate less headaches
high less headaches

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70
Q

how long does it take adenosine to up regulate receptors in number and sensitivity

A

as little as 2 cups of coffee per day for 5 days

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71
Q

T: coffee withdrawal condition marked by fatigue, flushing, nausea, anxiety, and headache.

A

abstinence syndrome

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72
Q

what causes abstinence syndrome

A

dilation of blood vessels in brain

inhibitory actions of more adenosine

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73
Q

inhibitory actions of adenosine on the release of other neurotransmitter molecules, including ..4

A

serotonin, norepinephrine, acetylcholine, and dopamine

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74
Q

what does caffeine do to peeing

A

more pee
less sensitive to full bladder
more flow and rate

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75
Q

how can you explain the diuretic effects of coffee

A

adenosine regulates kidney function

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76
Q

how can the confusing positive and negative subjective effects of caffeine be explained

A

depends on conditions

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77
Q

what conditions make for positive effects

A 
if have been not using coffee (not from withdrawal though)
low doses 
positive reinforcer (genetic?)
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78
Q

how do the subjective effects of theobromine compare o caffeine

A

same effects to less extent
same quickness of effects
bad effects 5- 10 h later not like caffeine

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79
Q

how was the subjective experience of caffeine on cacaine usurers different

A

There was a dose-related increase in rat-ings of “liking,” “drug effect,” “high,” and “good effects.” thought it was cocaine

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80
Q

what does high doses of caffeine feel like

A

anxiety and panic

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81
Q

why does high caffeine cause anxiety

A

particular A2c receptor in some peoples genes (due to effect on adenosine receptors)

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82
Q

what does glucose do when it interacts with caffeine

A

reduce hostility effect of caffeine but increase tension effect of caffeine

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83
Q

The addition of … counter-acts caffeine’s stimulatory impact on mood, fatigue, alert-ness, and vigor

A

taurine

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84
Q

In combination with caffeine, …, which is also present in tea, increases alertness and decreases head-ache

A

L-theanine

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85
Q

in energy drinks: …, is often taken in herbal-supplement capsules and is associated with subjective improvements in well-being, anxiety, depression, energy, and alertness

A

Ginkgo biloba

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86
Q

in energy drinks: … has been found to increase anxiety and panic

A

Yohimbine

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87
Q

why can’t we trust participants subjective reports of cognitive effects of caffeine

A

they have better mood and confidence so will think they preformed better without supporting results (no better on go no go task

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88
Q

what are the effects of coffee withdrawal

A

higher levels of sleepiness, lower mental alertness, and performed more poorly on reaction time and recognition memory tasks

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89
Q

does drinking caffeine have an impact on cognitive performance for non users

A

no just sleepiness due to anxiety (better cog performance in reg users due to return to baseline)

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90
Q

Researchers often find that caffeine is capable of
reversing decrements in performance caused by boredom and fatigue, certain drugs, caffeine withdrawal, and even the common cold

A

t

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91
Q

Caffeine has what 2 positive effects

A

improves attention and speeds both simple and choice reaction times.

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92
Q

how does adding glucose to caffeine change cognitive impacts

A

increase sustained attention and improve verbal memory vs only improving reaction time in just café’s

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93
Q

… in combi-nation with caffeine, has been found to reduce symptoms of caffeine withdrawal

A

Taurine,

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94
Q

caffeine alone decreased mental fatigue and improved informa-tion processing, while the addition of … further enhanced cognitive performance, as demonstrated by improvements in reaction time, working memory, long-term memory, and a decrease in headache

A

L-theanine in tea

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95
Q

caf-feine lowers the acoustic arousal threshold while sleeping so that people wake up more easily in response to a sound in the night.

A

t

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96
Q

does tolerance influence how disturbing can is to sleep

A

yes less disruptive (at first very disruptive

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97
Q

T: is a sleep-inducing center. When it is active, it causes sleep by generating synchronous activity in the cortex, which shows up on an EEG as slow waves

A

ventrolateral preoptic nucleus (VLPO)

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98
Q

are the wake or sleep centres in coms with the cortex

A

flip flops between them

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99
Q

how does Adenosine influence sleep and wake centres

A

a buildup of adenosine is one trigger that can activate the sleep cen-ter= caffeine blocks this activity

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100
Q

is caffeine a reinforcer

A

yes

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101
Q

what changes the reinforcing value of caffeine

A

your caf history

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102
Q

people don’t show café’s preference if you haven’t had coffee in past week

A

t

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103
Q

people actively avoid caffeine withdrawal and seek the effects of caffeine.

A

t

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104
Q

what factors contribute to the reinforcing properties of caffeine (how likely you are to choose it)

A

dependance to avoid withdrawal
positive effects
dose
task requirements

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105
Q

Coffee drinkers show a low-ered risk of developing type 2 diabetes.

A

t but decaf did too…

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106
Q

benefits of coffee consumption

A

diabetes
weight loss
cancer prevention
less coronary heart disease

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107
Q

why weight loss

A

increase metabolic rate energy expenditure, lipid degeneration, and thermogene-sis

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108
Q

dangers of caffeine consumption

A

cardiac disease

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109
Q

how does how you prepare coffee influence heart disease

A

One study has shown that boiled coffee contains a substance that raises cholesterol levels, but filtered coffee does not contain this factor

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110
Q

a positive relationship between caffeine consumption and cardiovascular disease, but only in indi-viduals with …

A

“slow metabolizing” form of the CYP1A2 enzyme gene

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111
Q

common adverse reactions to energy drinks?

A

Common reactions include elevations in blood pressure and heart rate, and minor cognitive effects such as insomnia

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112
Q

what are the hazards of standard consumption of energy drinks

A

flushing, headache, dizziness, tremor, hyperventilation, renal failure, vomiting, diarrhea, incontinence, fluctuations in blood pressure, fainting, anaphylactic shock, heart palpitations, chest pain, heart attack, hemorrhage, stroke, disorientation, spontaneous abortion, depression, anxiety, aggression, blindness, deafness, hallucinations, and convulsions

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113
Q

if energy drinks have same caffeine as cup of coffee why the extreme effects? 4

A

consumed rapidly
adol and young adults
can’t confirm caffeine intake due to other caffeine substances not listed
correlated with doing stupid sit

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114
Q

how much caffeine will kill you

A

150–200 mg/kg of body weight= 5000 to 50,000mg (Hodgman, 1998) or about 80–100 mg of caffeine per liter of blood

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115
Q

addition of taurine decrease caffeine fatalities

A

f The addition of taurine, for instance, to caffeine potentiates increases in blood pressure and caffeine-induced cardiac muscle contraction

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116
Q

how does caffeine kill you 3

A

ventricular fibril-lation, convulsions, and/or respiratory collapse.

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117
Q

does APA say there’s such thing as caffeine use disorder

A

intoxication and withdrawal syndromes, but excludes from potentially causing a “use disorder.” (WHO includes caffeine dependance syndrome)

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118
Q

3 criteria that must be met to prove can use disorder

A

(1) a persistent desire or unsuccessful efforts to reduce or control caffeine use; (2) continued caffeine use despite it causing or exacerbating an existing physical or psychological problem; and (3) withdrawal symptoms upon cessation or reduction of caffeine intake.

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119
Q

caffeine produces symptoms of intoxication: how?

A

restlessness, nervousness, excitement, insomnia, flushed face, diuresis, gastrointestinal distur-bance, muscle twitching, rambling flow of thought and speech, tachycardia or cardia arrhythmia, periods of inex-haustibility, and psychomotor agitation

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120
Q

Chronic administration of caffeine causes an upregulation in both the number and sensitivity of …

A

adenosine receptors

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121
Q

caffeine has less effect on heavy drinkers of cof-fee than on nondrinkers.

A

t

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122
Q

individuals who are most resistant to the effects of caffeine might also be the ones who become heavy coffee drinkers.

A

maybe but might be tolerance

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123
Q

how long till tolerance

A

The sleep-disrupting effects of caffeine show toler-ance within 7 days and the subjective effects are tolerated within 4 days

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124
Q

The effects of caf-feine on the body also build tolerance at different rates

A

t

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125
Q

Caffeine withdrawal symptoms include: …7

A

headache; fatigue or drowsiness; dysphoria, depressed mood, or irritability; difficulty concentrating; and flu-like symptoms including nausea, vomiting, or muscle pain and stiffness

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126
Q

Like …, withdrawal is feature of drug dependence.

A

tolerance

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127
Q

most common coffee withdrawal symptom?

A

headache

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128
Q

higher dose = what effect to withdrawal

A

faster tolerance

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129
Q

how long does withdrawal last

A

2-9 days

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130
Q

how long can withdrawal headaches last

A

up to 3 weeks

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131
Q

is it likely that caffeine use disorder will gain equal footing with other substance use disorders contained in the DSM?

A

no big business and is so widespread in normal functioning people

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132
Q

how can you take meth

A
  • orally
  • injected
  • snorted
  • smoked
  • anal and vag suppository
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133
Q

Following oral administration, meth-amphetamine bioavailability is ~…%. Its psychoactive effects can be felt within about …minutes following ingestion and reach their peak at about … hours.

A

67
20-60
3

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134
Q

when meth is smoked These routes result in drug bio-availability of ~…%
peak subjective effects?
peak blood level?

A

80–100
15 -20 min
2- 3 hours

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135
Q

When snorted, cardiovascular and peak sub-jective effects of methamphetamine are felt within … minutes, though peak blood plasma concentrations are reached nearly … hours later

A

5–15

4

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136
Q

why the difference between subjective effects and peak plasma in meth

A

acute tolerance

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137
Q

meth injection..

subjective effects?

A

10 min (2 min for cardiovascular effects)

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138
Q

how long does effects of meth last

A

up to 8 hours

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139
Q

how efficient is chewing the plant route of admin for cathinone

A

highly efficient; nearly 90% of plant constituents are released by chewing

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140
Q

chewing cathinone subjective effects? peak blood level?

A

begin at 30–60 minutes of chewing, as blood levels of cathinone begin to rise, and last for about 3 hours. Peak blood plasma concentrations are attained within about 1.5–3.5 hours

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141
Q

how do cathinones compare to amphetamines

A

Compared to the amphetamines, cathinones are less lipo-philic and therefore less able to penetrate the blood–brain barrier, requiring higher doses to produce reinforcing effects

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142
Q

… is pro-duced as a white or off-white powder that is most com-monly snorted

A

Methcathinone

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143
Q

Cocaine has a pKa of …

A

8.6

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144
Q

It is also common for those who self-administer coca in this way to mix the leaves with wood ashes or ground shells, which are alka-line why is this beneficial for cocaine injestion

A

raises the pH of the saliva and the digestive tract, consequently reducing drug ionization and increasing its absorption

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145
Q

is cocaine ever consumed orally

A

only when chewing not pure cocaine

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146
Q

Peak blood plasma levels of cocaine are reached within about… minutes to …hours of chewing

A

25 min to 2 hours

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147
Q

3 ways cocaine is taken

A

to improve absorption and enhance subjective effects, it is nearly always injected, snorted, or smoked.

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148
Q

why is cocaine rarely smoked

A

Because heat degrades the drug before it reaches the point of vaporiza-tion

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149
Q

why add Hcl salt like baking soda to cocaine before smoking

A

will free the HCl base from the salt, thereby removing the ionic charge from the molecules of cocaine, and increasing its lipid solubility. When the water evaporates, crystalline chunks are left

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150
Q

benefits of having cocaine in rock from

A

has a much lower melting point and can be heated in pipes or other devices, and its vapors inhaled.

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151
Q

When injected intravenously or smoked as crack,
peak blood plasma levels of cocaine are reached very quickly, within … minutes subjective effects are felt within… minutes of smoking crack and within … minutes of injecting cocaine snorting within…

A

2–5
1–2
3–4
10-15

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152
Q

does smoking or snorting crack lead to more bioavalibiility

A

snorting nothing lost as smoke

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153
Q

The absorption of methylphenidate varies consider-ably between individuals. name 2 ways

A

bioavailability

development

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154
Q

how readily do amphetamines cross the blood brain barrier

A

easily

155
Q 
put in order of highest to lowest concentrations of metham in the body 
lungs 
liver
heart 
pancreas
brain
A

The highest concentrations of metham-phetamine occur in the kidneys and lungs, followed by the stomach, pancreas, spleen, and liver, with lower concentra-tions in the heart and brain

156
Q

when are peak brain concentrations when smoking or injecting methamphetamine stimulants

A

9 min

157
Q

peak brain concentrations for cocaine?

A

concentrate more in brain = 4.5 min

158
Q

a greater total percentage of a cocaine dose enters the brain compared to a dose of methamphetamine

A

t

159
Q

oral vs injection peak brain concentration for methylphenidate

A

oral 1 hour

injection 8-20 min

160
Q

The excretion of amphetamines from the body depends a great deal on the ..

A

pH of the urine.

161
Q

how does Ph of urine effect?

A

more acidic= ionized and excreted

basic= drug reabsorbed and dealt with by liver

162
Q

what does the acidity of unine do to half life

A

more acidic decreases half life

basic prolongs it

163
Q

Approximately …% of a dose of amphetamine is excreted unchanged in urine

A

30–40

164
Q

amphetamines have behaviourally active metabolites

A

t but don’t contribute to subjective effects

165
Q

all the ways amph is eliminated

A

urine
sweat
saliva
liver!!!!

166
Q

is the half life longer for oral/ intravenous or snorted/ smoked

A

longer in snorted or smoked = less quick effects

167
Q

Approximately 70% of a dose of methamphetamine is excreted in urine within 24 hours what are the 3 things being excreted

A

unchanged methamphetamines
metabolites
amphetamine (from most to least)

168
Q

how long metham detectable in urine

A

1 week metabolites longer

169
Q

The metabolism of methamphetamine doesn’t appear to be altered by repeated drug use what does this tell us

A

tolerance is not enzymatic (pharmacokinetic) but pharmacodynamic

170
Q

how does cocaine half life compare to amphetamines

A

short ! 60 min

171
Q

what does half life depend on

A

route of admin
individual differences
ph of urine

172
Q

intravenous vs intranasal half life for cocaine?

A

longer in nasal longer again in oral

173
Q

how much cocaine excreted unchaged in urine

A

not much!

174
Q

how long canine detectable in urine

A

depends on route but 1.5- 3 days unless chronic doses 10 days

175
Q

The half-life of methylphenidate is age-dependent what’s Dif

A

shorter in kids 2.5 vs 3.5 hours

176
Q

how is methylphenidate excreted

A

inactive metabolite

177
Q

what is common to all psychomotor drugs

A

ability to impact neurotransmission at the monoaminergic synapses

178
Q

Moneraminergic: what are the 5 monoamine neurotransmitters

A

serotonin, dopamine, norepinephrine, epinephrine, and histamine.

179
Q

what is neuropharocology

A

the study of how drugs affect cellular function in the nervous system, and the neural mechanisms through which they influence behavior.

180
Q

T: the study of how drugs affect cellular function in the nervous system, and the neural mechanisms through which they influence behavior.

A

neuropharocology

181
Q

Following monoamine release and receptor-activation,

neurotransmission is terminated both by …2

A

the activity of spe-cific enzymes in the synaptic cleft

the reabsorption of neurotransmitter molecules into the presynaptic neuron.

182
Q

what enzymes terminal activity in cleft

A

monoamine oxi-dase (MAO) and catechol-O-methyltransferase (COMT)

183
Q

Reabsorption is achieved via special reuptake transporter molecules called …

A

monoamine transport-ers (MATs). = large protéine molecules on pre terminal

184
Q

Each monoamine has its own special transporter

A

t but MATs are structurally very similar to one another and are therefore capable of transporting molecules of each other’s neurotransmitter but lower affinity for them

185
Q

MATs belong to a family of transporter proteins called

…-dependent substrate-specific neuronal membrane trans-porters.

A

Na+/Cl

186
Q

how do NA cl dependant substrate-specific neuronal membrane trans-porters. use the gradient

A

use the power of the ionic gradient that exists between the outside and inside of a neuron to transport molecules of neurotransmitter from the synaptic cleft into the presynaptic axon terminal

187
Q

T: —a receptor located on the outer mem-brane of the transporter complex that binds its relevant monoamine

A

substrate recognition site

188
Q

Because the concentration of any monoamine will be much higher inside the axon terminal relative to outside in the synaptic space, simple gradient forces will not move the monoamine to the inside of the cell. how is this counteracted

A

MATs additionally bind Na+ and Cl-ions, which form a chemical complex with the monoamine, and rely on the motive force of the inward-directed Na+ ion gradient to transport molecules of monoamine into the neuron, against their own outward-directed concentration gradi-ent

189
Q

When a molecule of monoamine binds to its recogni-tion site on the transporter, a conformational change is trig-gered that causes the MAT to shift from an …

A

outward-facing to an inward-facing conformation

190
Q

describe the normal operation of a MAT protien

A

A molecule of monoamine neurotransmitter attaches to the MAT and is moved into the cell. This reduces the concentration of monoamine molecules in the
synaptic cleft. Once inside the cell, the monoamine is transported into the synaptic vesicle by a vesicular monoamine transporter 2 (VMAT2).

191
Q

what stimulant is a MAT reuptake blocker 2 (blocks keeping inward facing)

A

cocaine methylphenidate

192
Q

how do amphetamines work on MAT

A

substrate-releasing agent

193
Q

how do substrate releasing agents work

A

Molecules of the substrate-releasing agent are transported across the neuronal membrane by the MAT. Once inside the cell, they are taken into synaptic vesicles and subsequently reverse VMAT2 action, causing a release of stored monoamines into the cytosol of the axon terminal. Substrate-releasing agents also provoke a reversal of MAT action and cause the channel of the MAT to stay open, allowing monoamines to diffuse rapidly into the synaptic cleft.

194
Q

T: The process of packaging monoamine molecules in vesicles is accomplished by the action of another trans-porter, one that is embedded in the membrane of the synap-tic vesicle.

A

VMAT2 vesicular monoamine transporter 2

195
Q

Psychostimulant drug molecules have physico-chemical properties similar to those of the monoamine neurotransmitters. how does this change there function

A

competitive substates = alter function at MAT and VMAT2

196
Q

Cocaine and methylphenidate are equally potent inhibitors of DATs.

A

t

197
Q

at least …% of transporters must be blocked for users to experience a cocaine-induced high. what receptor>

A

47

dopamine

198
Q

other than dopamine what else does cocaine block

A

NE and 5-HT more than DA

199
Q

what are the 2 dopamine systems

A

motor activity and reinforcement and motivation

200
Q

At high doses, many of the monoamine reuptake inhibiting compounds actually produce dysphoric and aversive effects

A

t

201
Q

Bupropion is rather similar to cocaine and methylphenidate, in terms of its potency as a DAT inhibitor, yet its administration does not increase sub-jective “drug liking” what does this suggest about cocaine

A

cocaine and methylphenidate may have an additional, long-overlooked mechanism of action.

202
Q

what is a inverse agonists

A

a ligand that binds to the same receptor-binding site as an agonist and not only antagonizes the effects of an agonist but, moreover, exerts the opposite effect by suppressing spontaneous receptor signaling

203
Q

how does cociane and methelphenidates compare with DAT in binding affinity

A

6-7 times greater

204
Q

how do receptor response differ for dopamine on DAT compared to cocaine and methylphenidate on DAT

A

dopamine: recapture of monoamine from cleft into cell
cocaine: opposite conformational shift to keep monoamine in synapse during AP

205
Q

would a pure competitive DAT inhibitor create more or less effect compared to DAT inverse agonists like cocaine

A

less = no influx of Dopamine out of the cell

206
Q

would a pure competitive DAT inhibitor (bupropion) create more or less effect compared to DAT inverse agonists like cocaine

A

less = no influx of Dopamine out of the cell

207
Q

2 amphetamines?

A

l-and d-isomers, as well as methamphetamine

208
Q

amphetamines are structural analogs of monoamine NT, what is the relationship between monomines and them

A

compete for transport into cell (regulated by concentration)

209
Q

how do amped enter presynaptic neuron?

A

binding to a transporter protein, along with Na+ and Cl-ions

210
Q

why don’t cocaine and methylphenidate go into presynaptic neuron

A

too large to pass through transporter

211
Q

how are mono effected by amphetamines

A

slowed transport into pre cell due to competition

212
Q

increasing concentration of amph increases …

A

drug molecules that get inside cell

213
Q

amph and methamphetamine are best at inhibiting which receptor? NET, DAT or SERT

A

NET most potent, DAT then SERT

214
Q

how does the function of d-amphetamine vs l-amphetamine relate to their behavioural effects

A

l= less effective in DA and NE reuptake and 5 HT

D: better at DA less good at NE

215
Q

how do amphetamines affinity for VMAT2 influence monotones concentration

A

prevent the transport of mono-amines from the cytosol into vesicles, causing a buildup of unpackaged neurotransmitter molecules in the axon termi-nal.

216
Q

how do amph release mon into vesicle

A

distrust PH = release into cell due to higher concentration in cell due to reversal of VMAT2

217
Q

why are amph considered competitive substrate-releasing agents.

A

by causing reverse transport of mono

218
Q

why does Na+ plays a role in the displacement of monoamines

A

every molecule of amph getting in comes with a few NA = gradient doesn’t allow for more monamines

219
Q

AMPH disruption of Na+ distri-bution, combined with the outward monoamine gradient, forces a …

A

reversal in the direction of transporter action. = Nt out of cell

220
Q

second proposal for how amph release monodies

A

A second mechanism has also been proposed whereby amphet-amines induce rapid, brief bursts of monoamine efflux through the transporter protein, which acts momentarily as an open channel. This allows monoamine to flow out of the cell at a high rate

221
Q

Methamphetamine is less potent than d-or l-amphetamine

A

f more

222
Q

another effect exerted by the amphetamines is an inhibition of activity of MAO, how does this effect monomies

A

the enzyme that normally degrades any molecules of monoamine that float free in the cytosol of the cell

223
Q

what’s the difference between substrate releasing agents and reuptake inhibitors in terms of impact

A

autoreceptors shut down substrate release for classic inhibition but not for substrate melee

224
Q

all these amph reactions create what effect

A

rapid huge dopamine concentration = reinforcing and addictive

225
Q

because cocaine blocks SERTs and NETs in the same way that antidepressants do, it has have antidepressant properties

A

f cocaine dependence is strongly associated with depression

226
Q

…… are structurally similar

to amphetamine and methamphetamine, so it is no sur-prise that their effects are also analogous.

A

cathinone and methcathinone

227
Q

both cathinones and amphet and methamphetamines drugs act as monoamine substrate-releasing agents and enhance …, and, to a lesser extent,…

A

DA, NE

5 HT

228
Q

how do cat differ from amph

A

less potent

229
Q

difference between epinephrine and nonep?

A

While epinephrine has slightly more of an effect on your heart, norepinephrine has more of an effect on your blood vessels

230
Q

what is the effect of the Psychomotor stimulant drugs effect on epinephrine

A

strong cardiovascular effects that result from psychostimulant use

231
Q

why is cocaine an anesthesia

A

cocaine has the ability to block Na+ ion channels in cell membranes, which prevents the conduction of action potentials along nerve axons

232
Q

forgetting of what they learned when the effects of the drug wear off, suggesting that amphet-amine causes ..

A

dissociation

233
Q

what NT plays largest role in discriminative effects of amph

A

dopamine

234
Q

what are unconditioned behaviours of amphetamines at low and high doses

A 
low= increase locomotion 
high= sterotyped behaviours = no purpose
235
Q

what other drugs in stem family produce unconditioned behaviour

A

Both khat and cathinone enhance aggressive behavior of isolated rats
methacatha

236
Q

T: a stereotypical motor behavior in which there is an intense fascination with repetitive handling and examining of mechanical objects, such as picking at oneself or taking apart watches and radios

A

punding

237
Q

Because psychomotor stimulants activate the …, they produce elevations in heart rate and blood pressure, increase body temperature, and cause pupil dilation

A

sympathetic nervous system

238
Q

psychomotors daalde or constrict everthing

A

dilate

239
Q

their ability to dilate made them useful to treat…

A

asthma

240
Q

When stimulants are used for their psycho-active properties, most of the sympathomimetic effects are considered unpleasant. what are some of these symptoms

A

abdominal cramps, nausea, vomiting, tremors, and exacerbate motor tics

241
Q

… has stronger CNS effects and fewer peripheral effects than d-and l-amphetamine or cocaine.

A

Methamphetamine

242
Q

what do they do for food consumption

A

decrease it compensated later with excessive eating

243
Q

these stem activate serotonin 5-HT1B and 5-HT2C receptors what is behavioural consequence

A

feelings of being full

244
Q

users are annoyed when pending is interrupted

A

t

245
Q

punding and stereotyped behavior are caused by stimula-tion of the …, which has input into the extrapyramidal motor system

A

nigrostriatal DA system

246
Q

everyone experiences pleasurable effects form amphetamines

A

f some say anxiety (those who like and want do it again)

247
Q

One of the most noticeable effects of the amphetamines is that they …

A

improve mood make people feel good

a clear, organized mind; and a desire to get to work and accomplish things

248
Q

These subjective effects peaked at .. hours for the amphetamines and at … hours for methylphenidate, and had largely disappeared by … hours, even when adminis-tered at the higher doses

A

2,3,5

249
Q

intense feelings of pleasure called rushes account for the general feeling good produced by amph

A

f different effect but depend on how fast drug gets to brain in what concentration

250
Q

rushes often have a … component

A

sexual (feels like orgasm)

251
Q

When cocaine is injected intravenously, its subjective

effects are identical to those of intravenously administered amphetamines

A

t but shorter acting

252
Q

3 main effects on subjective experience

A

feel talkative friendly
stimulated
like the drug

253
Q

Peak subjective ratings of “high” occur during the rush

A

f shortly after the rush dissipates

254
Q

how fast does tolerance to cocaine rushes happen

A

rapid but still feels good

255
Q

Subjective reports of “good” effect and “high” are greater after injecting it intravenously

A

f after smoking cocaine (faster peak)

256
Q

numbing sensation called the freeze can be felt within a couple of minutes for what cocaine route of admin

A

nasal

257
Q

Peak subjective effects are reached in just under 15 minutes for what cocaine route

A

nasal

258
Q

methylphenidate’s binding sites and mechanisms of action are nearly identical to those of cocaine so why the Dif effects

A

slower acting longer half life = less abuse

259
Q

subjective effects of Khat chewing

A

positive stim effects followered by agitation, restlessness, anxiety, and depression as the hours-long chewing session reaches its end but can’t sleep

260
Q

Humans can quite readily learn to discriminate amphet-amine and other psychomotor stimulants from a placebo and Dif stimulants

A

f only placebo

261
Q

what are stimulations effects on sleep

A

made to prevent fatigue = can create insomnia

262
Q

stim sensory effects? 2

A

amphetamines increase auditory and visual acuity

passage of time underestimated = seems longer

263
Q

go pills = amphetamines improve performance

A

no better than coffee but increase aggression and willingness to fight

264
Q

response speed and short-term memory, accuracy on boring tasks, sustained vigilance are better on amphetamines

A

t but worse when have to attend to more than one thing

265
Q

T: attention becomes overwhelmed and this decreases a per-son’s ability to gather information effectively. People focus attention on only one event and fail to notice other things happening in the environment

A

tunnel vision

266
Q

on what tasks do stimulants harm performance

A

tasks that require cognitive flexibility and the ability to adopt new strategies

267
Q

the performance enhancing properties of stem are better with higher dosages

A

f At higher doses, most of the simple beneficial effects of stimulants are lost and peo-ple become impatient, more easily distracted, and show impaired judgment.

268
Q

stem improve athletic performance

A

t = why its banned

269
Q

cold meds could give you stimulations false negatives why

A

act as bronchodilators and are found in cold prepara-tions, cough syrups, and decongestants

270
Q

do cold meds containing l-methamphetamine have any performance enhancing effects

A

no

271
Q

what are amphetamines influence on driving

A

more likely to be killed more than any other drug (less for cocaine)

272
Q

people on amphetamines are just as bad driving at night as in day

A

f worse in day due to more stimuli no effect on night driving

273
Q

6 effects of ADHD

A

response inhibition, vigilance, timing, working memory, planning, decision-making, and mem-ory storage

274
Q

how many ADHD kids have impulsivity into adulthood

A

Roughly 65% of individuals with ADHD in childhood or adolescence

275
Q

The estimated prevalence of ADHD in adults is somewhere between …

A

2 and 3%

276
Q

3 stimulants used to treat ADHD

A

d-amphetamine, then methylphenidate, and most recently lisdexamfetamine

277
Q

ADHD medications drugs primarily target …. systems (dopamine and norepinephrine), which are believed to be dysfunctional in individuals with ADHD.

A

catecholamine neurotransmitter

278
Q

Why do stimulants work of aa drug defined by hyperactivity

A

differences in resting catecholamine level

279
Q

methylphenidate and amphetamine are … blockers

A

catecholamine
competitively inhibit DAT and NET reuptake = more DA and NE in cleft
stimulate D2 autoreceptors
negative feedback reduce DA singling on post cell

280
Q

when stressed catecholamine hormone signals production what 3 NT

A

dopamine; norepinephrine; and epinephrine

281
Q

how do stimulants reduce background noise

A

steady vs tsk related firing when on drug

282
Q

Increases in extra-cellular dopamine levels is bad for ADHD

A

f might also enhance the motiva-tional salience of a cognitive task in which an individual is engaged

283
Q

The relationship between catecholamine activity levels and cognitive functioning follows an inverted U-shape curve what does this mean

A

deficits, as well as excesses, of DA and NE can impair cognition (bad to take if you don’t have. deficit)

284
Q

does Methylphenidate work for ppl whose DA is too low

A

no

285
Q

how is cognition effected if you don’t have ADHD and take pill

A

selective attention and distractibility

better sustained attention

286
Q

short term and LT memory is improved with methylphenidate

A

f no ST

some LT for people with severe deficits

287
Q

stim improve cog and behavioural flexibility

A

f

288
Q

unprescribed stimulants has been found to com-promise study habits, lower motivation, and contribute to attention problems

A

f

289
Q

T: cocaine is usually taken in large quantities for brief periods of time that are followed by periods of abstinence.

A

run–abstinence cycle

290
Q

most common drug mix is the a combination of cocaine (or amphetamine) and heroin. :T

A

speed ball

291
Q

what is so pleasant about the speed ball

A

heroin reduces the jitteriness that cocaine arouses by stim-ulating the sympathetic nervous system, and the cocaine diminishes the sleepiness or nod caused by heroin (cocaine often mixed with Benzos)

292
Q

pure cocaine has a long history of self admin

A

t but less so for pure cocaaine (run absent cycles more common)then oral cocaine

293
Q

what is amphetamines pattern of self admin

A

run ab cycles but depends on why your taking eg present sleep or pleasure

294
Q

In the 1960s, this pattern of use characterized the peak user or speed freak who might inject amphetamine every few hours for days on end. what is likely to happen on this run

A

amphetamines psychosis = punding and paranoia

eventual crash

295
Q

why recent increase in amphetamines use

A

adderall

296
Q

guess which line is what drug figure 10-4 p 236

A

..

297
Q

Andean Natives who reg-ularly chew coca leaves have few health problems.

A

t

298
Q

why might users have a yellow complexion

A

mild jaundice caused by liver disease.

299
Q

what happens with prolonged nasal use

A

ulceration of mucous membrane progress to the extent that openings appear in the septum (the membrane separating the nostrils).

300
Q

During runs, users don’t report discomfort

A

f disturb-ing physiological and psychological symptoms

301
Q

The most commonly experi-enced side effects of methylphenidate use in children include …

A

headache, dizziness, drowsiness, sleep disturbance, irritability, abdominal pain, nausea, vomiting, diarrhea, cough, motor tics, and an increase in blood pressure and heart rate.

302
Q

what does methlphen do to appetite

A

restricts it along with growth restriction

303
Q

In adults, the use of oral amphetamine for short peri-ods have what negative effects

A

restless dizzy confusion

304
Q

High-dose, chronic stimulant use has the potential to cause serious harm, especially if administered ..

A

intravenously

305
Q

high dose chronic use has what effects

A

heart rate
blood pressure = internal bleeding or hemorrhage
brain damage
depression when off drug

306
Q

why brain damage

A

rupture small blood vessels in brain

307
Q

Compared to amphetamine or cocaine, the use of … can be even more harmful, both in the short and long term

A

meth-amphetamine

308
Q

Methamphetamine abuse is associated with …, a deterioration of skeletal muscle

A

rhabdomyolysis

309
Q

what is meth mouth (can happen with other stimulants)

A

dental decay from dry mouth due tosympa NS activity and teeth grinding

310
Q

sensation of bugs on skin

A

formication

311
Q

Methamphetamine users report high levels of …, including depression, suicidal ideation, anxiety, psychosis, difficulty controlling anger, and violent behavior

A

psychiatric symptoms

312
Q

Chronic khat chewing hasn’t shown many adverse effects

A

f
heart problems gastrointestinal problems, urinary retention, hyper-thermia, blurred vision, dizziness, insomnia, headache, cog functioning, depression etc

313
Q

Chronic khat chewing hasn’t shown many adverse effects

A

f
heart problems gastrointestinal problems, urinary retention, hyper-thermia, blurred vision, dizziness, insomnia, headache, cog functioning, depression etc

314
Q

which stem has most neurotoxic effects on the brain

A

methamphetamine

315
Q

T: toxicity in which a biological, chemical, or physical agent produces an adverse effect on the structure or function of the central and/or peripheral nervous system.

A

neurotoxicity

316
Q

what region is most effected in brain by amphetamines

A

regions containing dopamine and Seretonin producing cells

317
Q

neurotoxic effects only occur from large doses

A

f Damage is more readily inflicted by large drug doses and binge-like intake, though a slower trajectory of escalating drug intake also results in deleterious effects

318
Q

The loss of DATs that occurs as a result of methamphetamine use could be caused by what 2 things

A

down regulation of transporter proteins or

dopamine cell degiation

319
Q

In addition to affecting dopamine cells in the …,

methamphetamine exposure can produce long-term dam-age to dopamine and serotonin cells within the …2

A

striatum

hippocam-pus and prefrontal cortex

320
Q

decreases in the expression of tyrosine hydroxylase and tryptophan hydroxylase from amphetamines use tell us what

A

enzymes involved in the biosynthesis of DA and 5-HT= less

321
Q

Methamphetamine-induced neurotoxicity is associated with the cognitive symptoms of drug abuse.

A

t but also the , subjective, and psychomotor symptoms

322
Q

The loss of dopamine cells in the striatum correlates with the presence and severity of 3

A

psychotic symp-toms, memory deficits, and impaired psychomotor coordi-nation.

323
Q

The severity of psychotic symptoms from methamphetamine os correlated with …

A

diminished DAT and SERT density

324
Q

Brain abnormalities resulting from methamphetamine abuse are permanent for life

A

persist well beyond the period of drug administration but recover with abstinence

325
Q

The degree to which … function recovers during abstinence is predictive of therapeutic outcomes.

A

striatal dopa-mine

326
Q

T: When taken in high doses or used frequently for extended periods, cocaine, khat, methamphetamine, and amphet-amine can elicit psychotic behavior in otherwise healthy people.

A

monomine psychosis

327
Q

how similar is mon psychosis to schiz

A

indistinguishable

328
Q

what are the positive symptoms of mon psycho

A

positive= auditory and visual hall

329
Q

which are positive vs negative symptoms
delusions of reference, persecution, and grandeur; odd speech; flattened affect anxiety and agitation; depression and extreme paranoia that sometimes evokes hostility and violence, triggered by a belief that danger is imminent.

A

delusions of reference, persecution, and grandeur; odd speech; anxiety and agitation; and extreme paranoia that sometimes evokes hostility and violence, triggered by a belief that danger is imminent.

330
Q

In countries such as Yemen and Ethiopia where khat chewing is customary, two forms of khat psychosis are rec-ognized.

A

manic psychosis

schizophreniform psychosis

331
Q

T: paranoid, persecutory, and referential delusions; thought alienation; auditory hallucinations; a tendency to isolate oneself from others; fear and anxiety; a hostile perception of the environment; and aggressive behavior

A

schizophreniform psychosis

332
Q

T:It is marked by hyperactivity, talkative-ness, shouting, grandiose delusions, flight of ideas and tangential thought processes, and a highly liable mood that fluctuates from euphoria to anger

A

manic psychosis

333
Q

The psychotic symptoms most frequently experienced by regular metham-phetamine users are …3

A

delusions, hallucinations, and odd speech.

334
Q

which halluncinations most common?

A

auditory
visual
tactile

335
Q

the symptoms of mono-amine psychosis are transient what does this mean

A

don’t have lasting effects and go away when you stop use (in some people they persist)

336
Q

how does relapse influence chronic users psychotic symptoms

A

In chronic methamphet-amine users, behavioral sensitization to the drug’s effects means that even a small dose is capable of triggering a relapse of psychotic symptoms

337
Q

Psychotic symptoms may also be triggered during periods of meth-amphetamine abstinence by environmental stressors

A

t

338
Q

Sensitization to methamphetamine psychosis is caused by what

A

neurotoxic effects = DAT density in striatum and prefrontal cortex

339
Q

what do psychomotor stimulants do to sex drive

A

rev it when doing drug disinterest when off

340
Q

what do psychomotor stimulants do to baby when pregnant

A

birth abnormalities

low birth weight, increased pregnancy complications, pre-term delivery, and perinatal infant mortality

341
Q

cocaine use causes this. the placenta detaches prematurely:T

A

abruptoplacental

342
Q

some evidence that prenatal exposure to cocaine affects …. 6

A

childhood IQ, short-term memory, and ver-bal reasoning, particularly in male offspring , more behavioural problems

343
Q

why might cocaine users be unable to stand up, or may collapse but not lose con-sciousness

A

Users who take large doses of cocaine commonly experience muscle weakness and respiratory depression

344
Q

what determines lethal dose 2

A

cardiovascular susceptibility and route of admin

345
Q

how much cocaine will kill average person

A

1200 mg when cocaine is taken intranasally (depends on how much in brain not dose)
140 and 1650 mg of drug taken orally methamphetamine

346
Q

2 phases of cocaine overdose

A
  1. excitement followed by vommiting headache convulsions

2. pass out, resritory depends and cardiac failure

347
Q

how long does death by cocaine take

A

Death may be very rapid, within 2 to 3 minutes, or it may take as long as half an hour

348
Q

Chlorpromazine, an antipsychotic, is also very effective as an antagonist of the toxic effects of cocaine

A

t

349
Q

certain individuals might be highly resistant to the euphoric effects of the drug are less likely to OD

A

f more likely to try and get the high

350
Q

T: ntense cardiovascular effects that can be fatal when the drug is injected or inhaled in concentrated form

A

cocaine sudden-death syndrome

351
Q

Common signs of methamphetamine overdose include

A

dilated pupils, shivering, high fever, hypertension, rapid or laboured breathing, chest pain

352
Q

Altered mental status is common in …poisoning and most often include agitation, suicidal ideation, and psycho-sis

A

methamphetamine

353
Q

overdose deaths have occurred after as little as .. mg of methamphetamine administered intravenously

A

20

354
Q

reasons for overdose fatalities? 7

A

most commonly result from multisys-tem organ failure, pulmonary congestion, cerebrovascular hemorrhage, and acute cardiac failure, though deaths have also been attributed to sepsis resulting from dirty injections and by asphyxia by aspiration of vomit

355
Q

what accounts for more than 40% of meth deaths?

A

homocide and suiside

356
Q

The subjective effects of amphetamine and cocaine tend to be greater when blood levels of the drug are rising compared to when they are falling what is this a sign of

A

acute tolerance

357
Q

T: With the pattern of use that occurs during bingeing cocaine quickly loses its ability to cause rushes and gradually becomes incapable of improving mood

A

coke out

358
Q

what develops acute tolerance what doesn’t

A

no for cardiovascular

yes for subjective effects

359
Q

why do runs come to an end

A

coke out= loss of subjective pleasure

360
Q

pre-exposure to amphetamine decreased the drug’s …, but not its …, as a discriminative stimulus

A

potency

effectiveness

361
Q

which amph and cocaine effects are short acting vs no tolerance

A

short: apetitite, heart and blood pressure, effects
no: sleep

362
Q

any sensitization with stimulations?

A

stereotypes behaviours and psychosis

363
Q

After a single dose of amphetamine or cocaine, the high is typically followed by a crash, is this withdrawal?

A

no, occurs quicker in cocaine vs amphetamines

364
Q

is there withdrawal with cocaine and amphetamines

A

After chronic heavy use, abrupt discontinuation of amphetamine or cocaine can last weeks to months

365
Q

what are symptoms of withdrawal

A

depression, increased appetite, insomnia anxiety, agitation, and panic; drug craving; and cog-nitive impairment

366
Q

Withdrawal from psychomotor stimulants can also

disrupt performance why?

A

reduced cortical activation

failure to activate ventromedial cortex

367
Q

after 1 year of amphetamines abstinence cortical activation returned to normal

A

f continued decreased in dorsolateral prefrontal cortical activation

368
Q

what are treatments

A

detox= acute withdrawal (few weeks

pharmacotherapies that treat withdrawal

369
Q

3 common behavioural treatments

A

cognitive behav-ioral therapy, contingency management, and community reinforcement

370
Q

T: teaches strat-egies for rational thinking, avoidance of maladaptive behavior, and relapse prevention

A

CBT very effective

371
Q

T: uses conditioned rewards, such as vouchers for goods and services as operant technique for abstinence

A

contingency management works better than com with rewards = in long run

372
Q

T: uses social rein-forcement, such as praise and encouragement from one’s family and social group

A

community reinforcement

373
Q

T: drugs should block with-drawal symptoms, reduce craving for psychomotor stimu-lants, and block the effect of a psychomotor stimulant should it be taken.

A

pharmacotherapies

374
Q

what are different drug pharmacotherapies 5

A 
moDafinil
bupropion 
methylphenidate 
oral D amphetamine 
naltrexone
375
Q

T: —it stimulates dopamine, norepinephrine, and glutamate

and histamine w limited abuse potential

A

modfinil

376
Q

how effective is modafinil

A

There have been encouraging but inconclusive results with cocaine treatment
x methamphetamines

377
Q

T: is an antidepressant. DAT and NET blocker Its ability to enhance dopamine transmission in the nucleus accumbens and prefrontal cortex is the proposed mechanism by which the drug may reduce craving and the cognitive deficits associated with withdrawal.

A

Bupropion only effective on meth with light users

378
Q

why does methylphenidate help stimulant addicts = reduces amphetamines and peth cravings

A

It is a cocaine-like blocker of DATs and NETs with little effect on SERTs and is reported to have less abuse potential than cocaine and the amphetamines

379
Q

T: Oral is a safer route of administration and dampens fluctuations in blood drug levels, which are what cause rushes and euphoria= decrease dependance in meth

A

oral D amphetamines

380
Q

T: is an opioid antagonist, and the endogenous opioid system is implicated as a mecha-nism of drug reward = amphetamines users

A

naloxone

381
Q

what treatments work best

A

behavioral and psychosocial

382
Q

what is the logic behind a immunization

A

stimulate the immune system to create antibodies that would bind to molecules of
cocaine. This would prevent the drug from passing through the blood–brain barrier to enter the central ner-vous system, thereby blocking its effect.

383
Q

One of the difficulties in developing a vaccine for a

drug is… 3

A

the immune system normally only creates antibodies for large protein molecules, but drugs like cocaine and methamphetamine are small non-protein mol-ecules.
need many antibodies
levels drop after a few moths

345A (20 decks)

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