Biology of Addiction Flashcards

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1
Q

defined Schedule I - V drugs

A
  • Schedule I: no accepted medical use
  • Scehdule II: high potential for abuse / dependence
  • Schedule III: moderate - low potential for abuse / dependence
  • Schedule IV: low potential for abuse / dependence
  • Schdeuld V: lower potential for abuse / dependence than IV
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2
Q

heroin is what schedule drug?

A

schedule I

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3
Q

marijauna is what schedule drug?

A

schedule I

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4
Q

methamphetamine is what schedule drug?

A

schedule II

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5
Q

methadone is what schedule drug?

A

schedule II

(is an opioid)

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6
Q

oxycodone is what schedule drug?

A

schedule II

(is an opioid)

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7
Q

methylphenidate is what schedule drug?

A

schedule II

(CNS stimulant)

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8
Q

xanax is what schedule drug?

A

schedule IV

(is a benzodiazepene)

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9
Q

ambien is what schedule drug?

A

schedule IV

(is a BZ like drug)

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10
Q

what are examples of schedule V drugs?

A
  • anti-diarrheals
  • anti-tussives
  • certain analgesics
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11
Q

which professions have a higher risk for drug abuse?

A

physicians

dentists

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12
Q

what are behavioral and pharmacological indicators of drug abuse?

A

Behavioral Indicators

  • Impaired control and function
  • Social impairment’
  • Risky use
  • DUI, HIV, hepatitis C, meth effects

Pharmacological Indicators

  • Tolerance
  • Withdrawal
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13
Q

discuss the players in the reward circuit?

A

VTA releases dopamine via the mesolimbic projection to the nucleus accumbens

“VTA-to-NAc”

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14
Q

opiates

  • MOA:
  • AEs
  • overdose treatment?
  • addiction treatment?
A
  • mu agonist
  • AEs:
    • constipation
    • respiratory depression
    • sedation
    • addiction
  • overdose treatment: competitive antagonists - naloxone, naltrexone
  • addiction treatment: agonists - methadone, buprenorphine
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15
Q

heroin

  • what kind of drug
  • MOA / PK
  • administration
  • AE
  • risk factors for addiction
A
  • drug: schedule I opioid
  • MOA/PK: hydrophobic mu eceptor angatonist → faster onset
  • administration: injection, smoking [spoon often used]
  • AE:
    • social - crime, unemployment
    • respiratory depression / constipation (opioid AEs)
    • HIV, Hep-B & C - from sharing needles
    • skin infections → heart lining & valve infection - from non-sterile needles
  • risk factors: previous abuse of precription opioids - major*
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16
Q
A

skin popping

from subdermal use ot heroin, cocaine

17
Q
A

bacterial colonization of tricuspid valve

IV heroin use

18
Q

which drugs are used to treat opioid overdose?

A

opiod receptor antagonists

  • naloxone
  • naltrexone
19
Q

which drugs are used to treat opiod addiction?

A

opiod agonists

  • methadone - full mu receptor agonist
  • buprenorphine - partial mu receptor agonist
20
Q

what is suboxone?

why is it useful?

A

a combination of buprenorphine and nalaxone

effective & safe teatment for addiction, since buprenorphine is a mu agonist and nalaxone is an antagonist

21
Q

what are the benefits of using buprenorphine as opposed to methadone in the treatment of opioid addiction?

A

is a partial agonist, therefore:

  • less abuse potential
  • lesser eventual withdrawal symptoms & craving
  • safer - lesser risk of respiratory depression*
22
Q

what is the treatment BZ withdrawal?

A
  1. put patients on long-duration BZs
    • chlorodiazpoxide
    • diazepam
  2. slowly taper dose
23
Q

ethanol acts at what receptors?

to have what effects?

A

potentiates:

  • GABAA → inc GABA
  • VTA → inc ACh
  • nucleus accumbens → inc DA

inhibits: NMDA, kainate → less glutamate

24
Q

what are the elimination kinetics of ethanol?

what does this mean?

A

zero order kinetics

can eliminate one drink per hour

25
Q

what is the “J-shaped curve” pertaining to alcohol consumption?

A

at certain small levels, consumption of alcohol may have benefits

  • small levels: decreased risk for coronary disease
  • high levels: increased risk for arrythmias
26
Q

list the key treatments for alcohol addiction

what is the MOA for each?

A
  • naltrexone - mu receptor antagonist
  • acamprosate - GABA enhancement, glutamate inhibition
  • disulfram - aldehydrate dehydrogenase inhibitor
27
Q

what is acamprosate?

A

a therapy for alcohol addiction

28
Q

what is disulfiram?

how does it work?

A

an alcohol addiction therapy

disrupts ethanol metabolism such that acetylaldehyde accumulates→ makes patient sick & want to throw up

29
Q

stimulants

  • include what drugs
  • what schedule
  • AEs
A
  • drugs: amphetamines, methylphenidate, methamphetamine, cocaine
  • schedule II
  • AEs (at abuse levels)
    • social - unemployment / crime
    • physical
      • meth mouth: tooth decay of buccal / interproximal surfaces of teeth
      • psychosis
      • skin infections
30
Q

“meth mouth”

  • presentation
  • pathophysiology
  • medical intervention
A
  • presentation: specific pattern of tooth decay affecting:
    • buccal surfaces
    • interproximal surfaces - anterior teeth
  • pathophysiology: multifactorial
    1. poor oral hygeine → bacterial overgrowth → acid production
    2. vasoconstriction from amphetamines → xerostemia
  • medical intervention:
    • take opportunity to educate on risks / rehabilitation programs
    • postpone dental trx until abuse is controlled
31
Q

outline proper dental intervention for a patient with “meth mouth”

A
  • post-pone tx until abuse is controlled
  • if the pt has used methanphetamine within the last 24 hrs use LA without epinephrine*
    • amphetamines + epi → SNS drive to CV system → cardiac events