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Neuro-pharmacology > Amphetamines > Flashcards

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
Q

Amphetamines increase catecholamine release through four mechanisms 3

A

Altered catecholamine transport via TAAR1 signalling

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26
Q

Amphetamines increase catecholamine release through four mechanisms 4

A

MAO inhibition

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27
Q

Competitive inhibition of
DAT/NET

A

Dopamine and
amphetamine are both
substrates for the
dopamine transporter

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28
Q

At dopaminergic
terminals amphetamine
transport

A

competes with dopamine transport leading to elevated synaptic dopamine

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29
Q

Exchange transport at
VMAT

A

Once inside the cell, amphetamines is a substrate for the vesicular monoamine transporters (VMAT/VMAT2)

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30
Q

Amphetamines are
transported through VMAT
by

A

exchange with intravesicular dopamine, resulting in transport of
dopamine out of vesicles into the synaptic terminal.

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31
Q

Activation of TAAR1

A

increase the concentration of the associated monoamines in the synaptic cleft, causing the increased postsynaptic receptor binding.

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32
Q

TAAR1 signalling activates
protein kinase C (PKC) which

A

phosphorylates DAT.

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33
Q

Phosphorylated DAT reverses

A

the direction of dopamine transport (dopamine efflux transport) and is internalized (non-competitive reuptake inhibition).

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34
Q

Amphetamine competitively inhibits

A

reuptake through DAT

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35
Q

Amphetamine increases

A

cytosolic dopamine.

36
Q

Amphetamine increases DAT
internalization and

A

d induces dopamine
efflux by activating TAAR1.

37
Q

Additionally at higher doses amphetamines
inhibit

A

MAO, decreasing intracellular
dopamine breakdown.

38
Q

Prolonged amphetamine use can lead to

A

psychosis

39
Q

In animals methamphetamine doses
result in long-lasting decreases in

A

DA, tyrosine hydroxylase, and DAT in the
striatum

40
Q

In animals methamphetamine doses
result in long-lasting decreases in DA,
tyrosine hydroxylase, and DAT in the
striatum - Histology shows degeneration of

A

DA fibers

41
Q

In animals methamphetamine doses
result in long-lasting decreases in DA,
tyrosine hydroxylase, and DAT in the
striatum - * Damage to 5-HT fibers in

A

neocortex, hippocampus, and striatum

42
Q

Methamphetamine HCl (crystal meth) is highly

A

acidic

43
Q

Smoking causes degradation of

A

tooth enamel * ‘Meth mouth’

44
Q

‘Meth mouth’ Exacerbated by

A

sympathomimetic and
stereotypic effects

45
Q

‘Meth mouth’ Exacerbated by y sympathomimetic and
stereotypic effects

A

Decreased salivation
Dehydration
Teeth grinding

46
Q

Clinical uses of amphetamines decongestants

A

Largely discontinued as decongestants
after abuse potential was discovered

47
Q
  • Pseudoephedrine
A

decongestant

48
Q

amphetamines still used to treat

A

narcolepsy

49
Q

Amphetamines most common treatment
for

A

attention-deficit/hyperactivity
disorders (ADHD)

50
Q

Widely used (illicit) as

A

nootropic drugs

51
Q

Widely used (illicit) as nootropic drugs

A

High use among University students to
improve studying

52
Q

ADHD characterised by

A

increased
locomotor activity and distractibility

53
Q

inattentive ADHD subtype

A

– characterised by
extreme difficulty in sustained attention

54
Q

Impulsive-hyperactive ADHD subtype

A

characterised by high impulsivity and
excessive motor activity

55
Q

Combined ADHD subtype incorporates both

A

inattentiveness and impulsive-hyperactivity

56
Q

ADHD is dominated by an

A

attentional
deficit

57
Q

Hyperactivity manifests from

A

distractability

58
Q

ADHD may occur through excessive

A

DAT activity resulting in dopamine
insufficiency

59
Q

DAT density increased in

A

ADHD adults

60
Q

Genetic evidence foe ADHD links some cases with

A

polymorphism in the DAT gene

61
Q

Enactogenic Amphetamines

A

MDMA, MDA, MDE

62
Q

MDMA became popular among psychotherapists
in the late 70’s and early 80’s

A

MDMA caused clients to become more
communicative, introspective, and empathic

63
Q

Pharmacokinetics of enactogens

A

Readily absorbed from GI
* Plasma levels peak after 2 hours
* Half-life of 8 hours
* Liver metabolism

64
Q

Pharmacokinetics of enactogens - drug effect (6)

A

Euphoria
Increased wakefulness
Increased endurance
sociability
empathy
Sexual arousal

65
Q

Mechanism of action -MDMA functions as
amphetamines but has increased
activity at

A

seratonergic neurons

66
Q

Enactogenic effects are modulated
by effects on

A

5-HT

67
Q

Sympathomimetic and stimulant
effects modulated by

A

NE

68
Q

Reinforcing effects modulated by

A

DA

69
Q

amphetamines have a high affinity for

A

TAAR1 and VMAT

70
Q

Affects 5-HT, NE, and DA levels at

A

synapses

71
Q

Weak agonist at postsynaptic

A

5-HT1 and 5-
HT2
receptors

72
Q

MDA has more potent effects at

A

5-HTR

73
Q

MDMA found to increase

A

oxytocin levels in
healthy volunteers

74
Q

Oxytocin increase correlated with

A

subjective social effects

75
Q

Adverse effects (6)

A

Increased heart rate
* Tremors
* Sweating
* Hyperthermia
Trismus
Bruxism

76
Q

Hyperthermia

A

potentially fatal
Exacerbated by physical activity (i.e.
dancing)

77
Q

Trismus

A

(tightening of jaw muscles)

78
Q

Bruxism

A

(grinding teeth)

79
Q

Considered a stereotyped behaviour

A

Bruxism

80
Q

Withdrawal

A

No medically serious withdrawal syndrome

81
Q

Withdrawal Some effects persist briefly after cessation (crash similar to cocaine) (8)

A

Trismus
* Depression
* Anxiety or paranoia
* Irritability
* Impulsiveness
* Restlessness – insomnia
* Memory impairment
* Anhedonia

82
Q

Anhedonia

A

reduced ability to experience pleasure.

83
Q

Persistent effects

A

Evidence in animals of persistent
damage to DA and 5-HT systems

84
Q

Drug classification is based partly on

A

demonstrations of 5-HT damage

85
Q

Persistent effects in humans chemical effects

A

Decreased 5-HIAA in CSF
* Decreased 5-HT transporter binding capacity
* Decreased hormone response to seratonergic signaling

86
Q

Persistent effects in humans cognitive effects

A

Memory, visual processing, sleep

87
Q

Persistent effects in humans Interpretations

A

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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