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PSYCH 478 > Amphetamine > Flashcards

Amphetamine Flashcards

1
Q

true or false - enactogens are readily absorbed from GI

A

true

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2
Q

does enactogens affect plasma levels

A

yes they peak after 2 hours

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3
Q

how is enactogen metabolized

A

through the liver by CYP450

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4
Q

where does MDMA have increased activity

A

at seratonergic neurons

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5
Q

_______ and stimulant effects are modulated by __

A

sympathomimetic ; NE

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6
Q

reinforcing effects are modulated by _____

A

dopamine

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7
Q

MDMA increased what hormone levels

A

oxytocin

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8
Q

what are the adverse effects of enactogens

A

increased HR, tremors and sweating and hypothermia

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9
Q

what is trismus

A

tightening of jaw muscles

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10
Q

what is bruxism

A

grinding teeth

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11
Q

true or false - trismus is a stereotypes behavior

A

false - bruxism

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12
Q

true or false - hyperthemia from MDMA can be fatal

A

true

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13
Q

true or false - there re serious withdrawal symptoms from MDMA

A

false - not medically serious

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14
Q

the crash of MDMA is similar to what other drug

A

cocaine

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15
Q

what are some persistent effects from MDMA use

A
  • > decreased 5-HIAA in csf
    -> decreased 5-HT transporter binding
    -> decreased hormone response to seratonergic challenge
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16
Q

Amphetamines are a large class of _________
originally based on the naturally occurring _____________.

A

stimulants; ephedrine

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17
Q

Amphetamine first synthesized in 1887, brought
to market in 1930s as ___________ as a
___________.

A

benzedrine; decongestant

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18
Q

What is the parent compound to the class of amphetamines?

A

dopamine

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19
Q

How are amphetamines administered? Which is the most common therapeutic route? Which is susceptible to binge use?

A
  • oral = therapeutic
  • IV or inhalant = binge
20
Q

What is the half-life of amphetamines? Is this shorter or longer than cocaine?

A

7-30 hours; longer than cocaine

21
Q

TRUE or FALSE: Amphetamine and methamphetamine are used
interchangeably in clinical context

A

TRUE

22
Q

methamphetamine vs methamphetamine HCl

A
  • methamphetamine: more potent; higher BBB permeability; illicit use
  • methamphetamine HCl: smoking (crystal meth)
23
Q

What are the behavioural effects of amphetamines (other than psychosis, punding, and formication)?

A
  • euphoria or exhilaration
  • heightened alertness
  • increased confidence
  • reduced fatigue (insomnia)
  • improved performance on repetitive psychomotor tasks (Stereotyped behaviour)
  • enhanced athletic performance
24
Q

Describe psychosis induced by amphetamine administration.

A
  • Drug-induced, particularly in chronic users
  • Indistinguishable from schizophrenia
  • Use precipitates psychosis in schizophrenia
  • Can persist beyond periods of intoxication
25
Q

What is punding?

A

stereotyped behaviours

26
Q

Describe punding induced by amphetamines.

A
  • useless repetitive tasks
  • abstain from eating, drinking, bathroom breaks
  • irritated or angry if interrupted
27
Q

Describe formication induced by amphetamines.

A
  • feeling of insects crawling on skin
  • common to pick at skin as a result
28
Q

Which nerve terminals do amphetamines act at? Which NTs are affected?

A
  • catecholaminergic nerve terminals
  • dopamine, norepinephrine (and 5-HT)
29
Q

Amphetamine have lesser effects on 5-HT except ____________ amphetamines.

A

enactogenic

30
Q

What are the 4 mechanisms by which amphetamines increase catecholamine release?

A
  1. competitive inhibition of DAT/NET
  2. exchange transport at VMAT
  3. altered catecholamine transport via TAAR1 signalling
  4. MAO inhibition
31
Q

How does amphetamine competitive inhibition of DAT/NET increase catecholamines?

A
  • dopamine and amphetamine are both substrates for DAT
  • amphetamine competes with dopamine transport –> elevated synaptic dopamine
32
Q

Describe how amphetamine exchange transport at VMAT increases chatecholamines.

A
  • amphetamine is substrate for VMAT/VMAT2
  • amphetamines transported through VMAT by EXCHANGE WITH INTRAVESICULAR DOPAMINE (i.e. dopamine goes out of vesicles, into synaptic terminal)
33
Q

How does amphetamine activation of TAAR1 lead to increased catecholamines?

A
  • amphetamines bind intracellular receptor (Gs/Gq) involved in monoamine regulation - TAAR1
  • TAAR1 –> PKC –> phos DAT –> dopamine EFFLUX –> non-competitive reuptake inhibition
34
Q

Provide a summary for how amphetamines increase catecholamines.

A
  • competitively inhibit reuptake through DAT
  • increase cytosolic dopamine
    levels by exchange transport at VMAT
  • increases DAT
    internalization and induces dopamine
    efflux by activating TAAR1
  • inhibit MAO (at high dose), decreasing intracellular
    dopamine breakdown
35
Q

Describe persistne effects of amphetamine use.

A
  • prolonged use –> psychosis
  • hallucinations and paranoia (resembling schizophrenia)
  • can occur outside of intoxication in chronic users
36
Q

In animals, methamphetamine doses result in long-lasting decreases in ______, ___________, and _______ in the striatum.

A

DA; tyrosine hydroxylase; DAT

37
Q

review slide 13 image

A

go look

38
Q

What form of amphetamins is in common use?

A

pseudoephedrine

39
Q

Why does smoking methamphetamine HCl degrade tooth enamel? What is this exacerbated by?

A
  • highly acidic; reduced self-care in heavy abusers
  • exacerbated by sympathomimetic and stereotypic effects (decreased salivation, dehydration, teeth grinding)
40
Q

What are some clinical uses of amphetamines? Which is most common? Which form is illicit?

A
  • narcolepsy
  • ADHD (most common)
  • nootropic; improve studying (illicit)
41
Q

What is ADHD characterized by?

A
  • increased locomotor activity and distractibility
  • difficult in sustained attention
  • high impulsivity
  • excessive motor activity
42
Q

Why are psychomotor stimulants effective in treating ADHD?

A
  • ADHD may occur through excessive DAT activity –> dopamine insufficiency
  • DAT density increased in ADHD adults
  • genetic evidence links some cases with polymorphism in the DAT gene
43
Q

What is an example of an enactogenic amphetamine? What behavioural effects are seen?

A
  • MDMA
  • communicative, introspective, empathic
44
Q

Where are enactogens readily absorbed from? When do plasma levels peak? What is the half-life? What enzyme does liver metabolism occur by?

A
  • GI
  • peak after 2 hours
  • half-life of 8 hours
  • CYP450 2D6
45
Q

What are the drug effects of enactogens?

A

*Euphoria
* Increased wakefulness
* Increased endurance
* Sense of well-being, sociability, and extraversion
* Sense of closeness, tolerance, and empathy to others
* Sexual arousal

PSYCH 478 (28 decks)

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