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PMCOL 305 > amphetamines > Flashcards

amphetamines Flashcards

1
Q

what is amphetamine (1 word)

A

stimulant

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2
Q

what is methamphetamine

A

amphetamine derivative that enters the brain more rapidly

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3
Q

what is crystal meth

A

methamphetamine hydrochloride crystals - smokable

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4
Q

what are the psychological effects of methamphetamine

A

euphoria, energy, alertness (same as cocaine)

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5
Q

what is punding

A

repetitive meaningless behaviours

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6
Q

what weird thing happens at high methamphetamine doses

A

punding

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7
Q

what causes punding

A

too much DA in basal ganglia

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8
Q

what is the role of the basal ganglia

A

voluntary motor control and action selection

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9
Q

what medical condition is punding often found in and why

A

parkinson’s patients if medicine drastically increases DA levels

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10
Q

what is a bad psychological effect of amphetamine

A

unprovoked aggression and violence

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11
Q

what % of people have engaged in violent behaviour or suicide with methamphetamine

A

43% and 27%

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12
Q

can methamphetamine cause paranoia and hallucination

A

yes

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13
Q

what is a weird PSYCHOLOGICAL effect of methamphetamines

A

delusions of parasitosis

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14
Q

do methamphetamines have local anesthetic actions

A

no

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15
Q

do methamphetamines do anything to the sympathetic stimulation

A

yes, like cocaine (increased HR BP insomnia)

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16
Q

what are some physiological effects of methamphetamine

A

increase BP HR, tremours, headache, sweating

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17
Q

what happens to body temperature with methamphetamine

A

hyperthermia

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18
Q

what 4 things can cause death from methamphetamine

A

renal and hepatic failure, strokes, seizures

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19
Q

are amphetamines natural synthetic or semi

A

purely synthetic

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20
Q

what are 6 ways that amphetamines have been used medically

A 
asthma
weight loss
depression
ADHD
narcolepsy
stimulant (soldiers)
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21
Q

what 2 structures is amphetamine similar to

A

NA and DA

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22
Q

which receptors do amphetamines interact with and why

A

same transporters as DA and other NTs because of close structural similarity

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23
Q

why is methamphetamine the amphetamine of choice (3)

A
  • extra methyl makes it easier to enter brain + more difficult to metabolize
  • less peripheral more CNS effects
  • smokeable
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24
Q

does amphetamine or methamphetamine have more CNS effects

A

methamphetamine

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25
Q

does amphetamine or methamphetamine have more PNS effects

A

amphetamine

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26
Q

does amphetamine or methamphetamine get in the brain easier

A

methamphetamines

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27
Q

does amphetamine or methamphetamine metabolized easier

A

amphetamines

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28
Q

why amphetamine easier to metabolize than methamphetamine

A

because meth has the extra methyl group

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29
Q

what form is meth smokable in

A

crystalline hydrochloride form

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30
Q

where does most methamphetamine come from

A

mexico

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31
Q

what is the starting molecule for methamphetamine synthesis

A

pseudophedrine

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32
Q

what kind of dangerous waste is made to make methamphetamine

A

lithium batteries, sodium, match heads (phosphorus), ammonia

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33
Q

how much water is made for every 1kg of produce

A

5-7kg

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34
Q

how much water is made for every 10kg of produce

A

50-70kg

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35
Q

what is a pro to the shake and bake / one pot method of making meth

A

less pseudophedrine is needed

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36
Q

what is a con to the shake and bake / one pot method of making meth

A

can cause explosions, flash fires if O2 enters bottle too quickly

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37
Q

the pattern of use for meth is similar to what drug

A

cocaine (orally, snorted, smoked, injected)

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38
Q

does meth or cocaine last longer

A

meth

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39
Q

does meth or cocaine have to be administered more often

A

cocaine

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40
Q

why does meth make a rapid tolerance

A

because there is rapid NT depletion with high doses

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41
Q

why is cocaines high shorter lasting than meth

A

because it doesnt stay in the brain for as long

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42
Q

which enzyme breaks down amphetamines

A

CYP2D6

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43
Q

what does CYP2D6 do to amphetamines

A

adds OH to make it more water soluble

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44
Q

which enzyme breaks down methamphetamines

A

CYP2D6

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45
Q

what does CYP2D6 break methamphetamines into

A

amphetamines or 4-hydroxymethamphetamine

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46
Q

what are the 3 metabolites of methamphetamines and amphetamines

A

4-HMA
4-HA
NE
(4-hydroxymethamphetamine, 4-hydroxyamphetaminem norephedrine)

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47
Q

what does norephedrine do

A

mimics the effects of adrenaline at adrenergic receptors (blood vessel effect)

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48
Q

what does 4-HA do

A

stimulates NA release, inhibits MAO, activates TAAR

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49
Q

what does 4-HMA do

A

MAYBE stimulates NA release, inhibits MAO, activates TAAR

50
Q

what does TAAR stand for

A

trace amine associated receptor

51
Q

what do 4-HMA 4-HA and NE do to the body (1 word

A

stimulation

52
Q

what % of Caucasians are deficient in CYP2D6

A

10%

53
Q

which metabolites stimulate NA release

A

4-HA and 4-HMA

54
Q

which metabolites inhibit MAO

A

4-HA and 4-HMA

55
Q

which metabolites activate TAAR

A

4-HA and 4-HMA

56
Q

which metabolites mimic effects of adrenaline at adrenergic receptors

A

norephedrine

57
Q

which NTs do amphetamines block the uptake of

A

DA NE and serotonin

58
Q

what is the main difference with cocaine and amphetamines when it comes to DA buildup

A

cocaine needs NT release but amphetamines dont need NT release / depolarization events

59
Q

do amphetamines need depolarization events for DA buildup to occur

A

no

60
Q

does cocaine need depolarization events for DA buildup to occur

A

yes

61
Q

what does VMAT stand for

A

vesicular monoamine transporter

62
Q

how is amphetamine transported into NT storage vesicles

A

VMAT

63
Q

what happens once amphetamines are pumped into nerve terminal

A

they are transported into vesicles

64
Q

besides the transporters, what other receptors may be affected by amphetamines

A

nicotinic acetylcholine receptors

65
Q

what are 2 ways that amphetamines enter the presynaptic terminals

A

transportation by DAT

diffusion across the membrane (high concentrations)

66
Q

what is the difference with amphetamines and cocaines interaction with DAT

A

amphetamines actually are transported into the nerve endings unlike cocaine which just inhibits DAT

67
Q

why can amphetamines go through DAT unlike cocaine

A

it is smaller and more structurally similar to DA

68
Q

what does MAO do

A

degrades DA NE E 5HT

69
Q

what happens once VMAT brings amphetamines into vesicles

A

they induce the vesicles to spew out DA into the cytoplasm

70
Q

what 2 things allow DA to accumulate in the nerve ending from amphetamines

A

1-vesicles spew out all DA

2- MAO is inhibited so it can’t break down the free DA

71
Q

what does interactions with TAAR cause

A

DAT pumps in reverse so that DA is pumped into the synapse

72
Q

what causes DAT to pump in reverse

A

amphetamines interactions with TAAR

73
Q

with amphetamines, what are 2 ways DA leaves the pre-synaptic neuron

A

1-DAT in reverse

2-diffusion

74
Q

does cocaine interact with TAAR

A

no

75
Q

what causes TAAR to let DAT run in reverse

A

G protein cascade, phosphorylation of DAT lets it be reversed

76
Q

does amphetamines or cocaine have a higher DA release in NAc

A

amphetamines

77
Q

what are 2 other pathways (besides dopaminergic) that gives the effect of amphetamines

A

noradrenergic and serotonergic pathways

78
Q

what is tyrosine hydroxylase

A

enzyme in DA and NA synthesis pathway

79
Q

what happens to tyrosine hydroxylase with amphetamine use and why

A

inhibited because the nerve endings see massive amounts of DA so you want to downregulate the synthesis pathway

80
Q

what does a single dose of amphetamines do to DAT function

A

decreases its function

81
Q

what does chronic amphetamine use do to DAT expression

A

less DAT expression on the cell-surface

82
Q

what does chronic amphetamines do to cell surface transporter expression

A

decreases - DAT and for NE too

83
Q

what causes the effects of less transporters on the cell surface from amphetamines

A

TAAR activation

84
Q

does amphetamines cause brain damage, what kind

A

yes, profound changes in brain structure

85
Q

what kind of terminals are reduced with amphetamine use

A

Dopamiergic, serotonergic and noradrenergic terminals are reduced

86
Q

with amphetamines, are Dopamiergic, serotonergic and noradrenergic terminals reduced temporarily or permanently

A

likely permanently

87
Q

what causes amphetamine damage to brain cells

A

free DA forming ROS when metabolized by MAO (even though it is inhibited) which causes damage of cell membranes proteins and mitochondria

88
Q

what does excessive glutamate release cause

A

toxic environment that leads to neuronal cell death (excitotoxicity)

89
Q

what do amphetamines do to glutamate release

A

cause excessive glu release

90
Q

what causes excitotoxicity

A

excess glu release

91
Q

does meth cause neuronal loss

A

yes

92
Q

where does meth cause neuronal loss

A

globally, but mainly in hippocampal, limbic and cingulate system

93
Q

what does the cingulate system do (4)

A

learning memory emotion motivation

94
Q

which type of meth users get the most significant neuronal loss

A

people will early onset schizo and dementia

95
Q

what kind of tests will show correlation with hippocampal volume loss

A

word-recall

96
Q

what happens to brain / long-lasting changes with amphetamine use

A

death of dopaminergic neurons

97
Q

what is brain damage from amphetamines similar to (which disease) and why

A

parkinsons because that is a loss of DA neurons

98
Q

is there an increased risk of parkinsons with cocaine use, how much

A

no none

99
Q

is there an increased risk of parkinsons with amphetamines use, how much

A

yes 76% increase

100
Q

what happens when amphetamines bind to nAChR (1st step)

A

they let Ca++ into the neuron

101
Q

what happens when Ca++ enters neuron from amphetamines activating nAChR

A

cascade of events leading to increased levels of ROS

102
Q

which receptor may be a leading factor in brain damage from amphetamines (like the cause of the damage)

A

nAChR - cascade of events leads to ROS release

103
Q

what happens with you use nAChR receptor blockers with amphetamines

A

there is less ROS damage and prevents some neuronal damage IN VITRO

104
Q

which specific nAChR subunit may be most implicated in ROS formation

A

alpha 7!!!

105
Q

which ion flows through when nAChR is acticated

A

Ca++

106
Q

what happens with increase Ca++ in ACh cells

A

triggers increased levels of ROS

107
Q

what are 5 symptoms of withdrawal from amphetamines

A

anhedonia, fatigue, mood volatility, vegetative state, intense cravings

108
Q

what is anhedonia

A

inability to feel pleasure

109
Q

what causes anhedonia in withdrawal

A

because tyrosine hydroxylase is inhibited so less DA is made

110
Q

how long can amphetamine withdrawal last

A

12 months

111
Q

what does length of amphetamine withdrawal link to

A

decree of brain damage/dysfuntion

112
Q

what may cause someone to never recover from amphetamines

A

if dopaminergic neurons were destroyed

113
Q

what are 2 possible causes of meth mouth

A

contaminants in meth, lack of saliva

114
Q

why may the contaminants in meth cause meth mouth

A

because many meth components are highly corrosive

115
Q

why does meth cause a lack of saliva

A

vasoconstriction in gums

116
Q

what causes vasoconstriction in gums

A

excess NA onto alpha1 receptors on blood vessels AND activation of inhibitory alpha2 presynaptic neurons in salivary glands

117
Q

what does amphetamine do to alpha1 (salivary glands)

A

excess NA stimulation causes vasoconstriction

118
Q

what does amphetamine do to alpha2 (salivary glands)

A

they are inhibitory presynaptic, so activating them reduces saliva flow

119
Q

what happens when alpha2 isnt activated (normal circumstances)

A

NA causes saliva flow

alpha2 is inhibitory presynaptic

120
Q

what does alpha2 activation in saliva glands cause

A

less saliva flows

PMCOL 305 (26 decks)

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