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Amphetamines Flashcards

1
Q

Amphetamines

A

large class of stimulants
originally based on the naturally occurring
ephedrine

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2
Q

Amphetamine first market product

A

Benzedrine as a
decongestant

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3
Q

Benzedrine came into regular use in
WWII for it’s

A

stimulant and performance
enhancing effects

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4
Q

Use became regulated in

A

60’s and 70’s as
addictive potential emerged

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5
Q

Remain in use in military

A

Canada’s first losses in Afghanistan were in
a friendly-fire incident blamed partly on the
US pilots use of amphetamines

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6
Q

amphetamines Typically taken

A

orally

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7
Q

in cases of abuse how in amphetamine taken

A

IV or smoking

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8
Q

Amphetamine and methamphetamine are used

A

interchangeably in clinical context

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9
Q

Methamphetamine

A

more potent and has higher
BBB permeability and is preferred for illicit use

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10
Q

Methamphetamine HCl

A

l is preferred for smoking
(crystal meth)

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11
Q

As with cocaine – oral route is

A

slowest, least
susceptible for abuse

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12
Q

amphetamine is metabolized in the

A

Liver

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13
Q

Much longer half-life than cocaine

A

7-30 hours

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14
Q

Susceptible to binge use

A

typically IV or inhalant

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15
Q

Susceptible to binge use – typically IV or inhalant

A

Often combined with depressants to limit anxiety
(mixed with barbiturates or heroin – ‘speedball’)

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16
Q

Behavioural effects (6)

A
  • Euphoria
  • Heightened alertness
  • Increased confidence
  • Reduced fatigue
  • Improved performance on repetitive
    psychomotor tasks
  • Enhanced athletic performance
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17
Q

Psychosis (3)

A
  • Indistinguishable from schizophrenia
  • Use precipitates psychosis in schizophrenia
  • Can persist beyond periods of intoxication
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18
Q

Punding – stereotyped behaviours (3)

A
  • Useless repetitive tasks
  • Abstain from eating, drinking, bathroom breaks
  • Irritated or angry if interrupted
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19
Q

Formication

A
  • Feeling of insects crawling on skin
  • Common to pick at skin as a result
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20
Q

Amphetamines act at

A

catecholaminergic nerve terminals

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21
Q

Amphetamines act at catecholaminergic nerve terminals

A

Dopamine
* Norepinephrine
* Lesser effects on 5-HT (exception being the enactogenic amphetamines)

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22
Q

Like cocaine, amphetamines are

A

reinforcing through effects on dopamine and are stimulant and
sympathomimetic through effects on norepinephrine

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23
Q

Amphetamines increase catecholamine release through four mechanisms 1

A

Competitive inhibition of DAT/NET

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24
Q

Amphetamines increase catecholamine release through four mechanisms 2

A

Exchange transport at VMAT

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25
Amphetamines increase catecholamine release through four mechanisms 3
Altered catecholamine transport via TAAR1 signalling
26
Amphetamines increase catecholamine release through four mechanisms 4
MAO inhibition
27
Competitive inhibition of DAT/NET
Dopamine and amphetamine are both substrates for the dopamine transporter
28
At dopaminergic terminals amphetamine transport
competes with dopamine transport leading to elevated synaptic dopamine
29
Exchange transport at VMAT
Once inside the cell, amphetamines is a substrate for the vesicular monoamine transporters (VMAT/VMAT2)
30
Amphetamines are transported through VMAT by
exchange with intravesicular dopamine, resulting in transport of dopamine out of vesicles into the synaptic terminal.
31
Activation of TAAR1
increase the concentration of the associated monoamines in the synaptic cleft, causing the increased postsynaptic receptor binding.
32
TAAR1 signalling activates protein kinase C (PKC) which
phosphorylates DAT.
33
Phosphorylated DAT reverses
the direction of dopamine transport (dopamine efflux transport) and is internalized (non-competitive reuptake inhibition).
34
Amphetamine competitively inhibits
reuptake through DAT
35
Amphetamine increases
cytosolic dopamine.
36
Amphetamine increases DAT internalization and
d induces dopamine efflux by activating TAAR1.
37
Additionally at higher doses amphetamines inhibit
MAO, decreasing intracellular dopamine breakdown.
38
Prolonged amphetamine use can lead to
psychosis
39
In animals methamphetamine doses result in long-lasting decreases in
DA, tyrosine hydroxylase, and DAT in the striatum
40
In animals methamphetamine doses result in long-lasting decreases in DA, tyrosine hydroxylase, and DAT in the striatum - Histology shows degeneration of
DA fibers
41
In animals methamphetamine doses result in long-lasting decreases in DA, tyrosine hydroxylase, and DAT in the striatum - * Damage to 5-HT fibers in
neocortex, hippocampus, and striatum
42
Methamphetamine HCl (crystal meth) is highly
acidic
43
Smoking causes degradation of
tooth enamel * ‘Meth mouth’
44
‘Meth mouth’ Exacerbated by
sympathomimetic and stereotypic effects
45
‘Meth mouth’ Exacerbated by y sympathomimetic and stereotypic effects
Decreased salivation Dehydration Teeth grinding
46
Clinical uses of amphetamines decongestants
Largely discontinued as decongestants after abuse potential was discovered
47
* Pseudoephedrine
decongestant
48
amphetamines still used to treat
narcolepsy
49
Amphetamines most common treatment for
attention-deficit/hyperactivity disorders (ADHD)
50
Widely used (illicit) as
nootropic drugs
51
Widely used (illicit) as nootropic drugs
High use among University students to improve studying
52
ADHD characterised by
increased locomotor activity and distractibility
53
inattentive ADHD subtype
– characterised by extreme difficulty in sustained attention
54
Impulsive-hyperactive ADHD subtype
characterised by high impulsivity and excessive motor activity
55
Combined ADHD subtype incorporates both
inattentiveness and impulsive-hyperactivity
56
ADHD is dominated by an
attentional deficit
57
Hyperactivity manifests from
distractability
58
ADHD may occur through excessive
DAT activity resulting in dopamine insufficiency
59
DAT density increased in
ADHD adults
60
Genetic evidence foe ADHD links some cases with
polymorphism in the DAT gene
61
Enactogenic Amphetamines
MDMA, MDA, MDE
62
MDMA became popular among psychotherapists in the late 70’s and early 80’s
MDMA caused clients to become more communicative, introspective, and empathic
63
Pharmacokinetics of enactogens
Readily absorbed from GI * Plasma levels peak after 2 hours * Half-life of 8 hours * Liver metabolism
64
Pharmacokinetics of enactogens - drug effect (6)
Euphoria Increased wakefulness Increased endurance sociability empathy Sexual arousal
65
Mechanism of action -MDMA functions as amphetamines but has increased activity at
seratonergic neurons
66
Enactogenic effects are modulated by effects on
5-HT
67
Sympathomimetic and stimulant effects modulated by
NE
68
Reinforcing effects modulated by
DA
69
amphetamines have a high affinity for
TAAR1 and VMAT
70
Affects 5-HT, NE, and DA levels at
synapses
71
Weak agonist at postsynaptic
5-HT1 and 5- HT2 receptors
72
MDA has more potent effects at
5-HTR
73
MDMA found to increase
oxytocin levels in healthy volunteers
74
Oxytocin increase correlated with
subjective social effects
75
Adverse effects (6)
Increased heart rate * Tremors * Sweating * Hyperthermia Trismus Bruxism
76
Hyperthermia
potentially fatal Exacerbated by physical activity (i.e. dancing)
77
Trismus
(tightening of jaw muscles)
78
Bruxism
(grinding teeth)
79
Considered a stereotyped behaviour
Bruxism
80
Withdrawal
No medically serious withdrawal syndrome
81
Withdrawal Some effects persist briefly after cessation (crash similar to cocaine) (8)
Trismus * Depression * Anxiety or paranoia * Irritability * Impulsiveness * Restlessness – insomnia * Memory impairment * Anhedonia
82
Anhedonia
reduced ability to experience pleasure.
83
Persistent effects
Evidence in animals of persistent damage to DA and 5-HT systems
84
Drug classification is based partly on
demonstrations of 5-HT damage
85
Persistent effects in humans chemical effects
Decreased 5-HIAA in CSF * Decreased 5-HT transporter binding capacity * Decreased hormone response to seratonergic signaling
86
Persistent effects in humans cognitive effects
Memory, visual processing, sleep
87
Persistent effects in humans Interpretations
No demonstration of effects of casual use * Confounded by coincident drug use * Impurities / adulterants in illicit drugs

Neuro-pharmacology (26 decks)

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