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Pharm Exam 3 > 43/44: Drugs of Abuse > Flashcards

43/44: Drugs of Abuse Flashcards

1
Q

define drug abuse

A

consumption of drugs without medical approval or supervision to achieve strong feelings of euphoria and reward ; use of a drug in a manner detrimental to the health and well-being of the drug user, other individuals or society as a whole

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2
Q

hallmark of drug addiction

A

compulsive drug use

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3
Q

when drug is necessary for normal physiological functioning =

A

physical dependence

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4
Q

pharmacokinetic v. pharmacodynamic tolerance

A

pharmacokinetic: increased drug metabolism results in decrease in the amount of available drug or duration of drug action at the target site
pharmacodynamic: CNS responds and adapts to presence of drug –> desensitization, down-regulation and/or internalization of receptors

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5
Q

compulsive drug use to induce pleasure and/or an escape from reality despite negative consequences

A

addiction

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6
Q

CNS mechanisms of psychological dependence

A

increased synaptic plasticity and DA release in the mesolimbic reward pathways

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7
Q

t or f: all drugs of abuse are addictive

A

false

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8
Q

all addictive drugs activate…

A

mesolimbic dopamine system –> reward pathway

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9
Q

DA neurons from the ventral tegmentum project to…

A

amygdala
nculeus accumbens
prefrontal cortex
hippocampus

all part of reward pathway

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10
Q

RR for CNS depressants and sedative/hypnotics

A

3

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11
Q

ETOH is a depressant –> ________. Why do we use it?

A

produces sedation and sleep

low doses of ETOH cause suppression of inhibitory systems and mild euphoria, which facilitates social interactions by reducing behavioral inhibitions and self-consciousness

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12
Q

basis for breathalyzer test

A

10% ETOH metabolized in GI tract and excreted through kidney and lungs

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13
Q

elimination of ETOH from the blood follows

A

zero-order kinetics

rate of elimination is independent of time and concentration of ETOH (constant amount eliminated per unit time )

one drink/hr approx

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14
Q

converts ETOH into acetaldehyde

A

alcohol dehyrogenase

part of alcohol metabolism

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15
Q

converts acetaldehyde to acetic acid

A

aldehyde dehydrogenase

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16
Q

MOA and use of disulfiram

A

inhibits ALDH and is used to encourag alcoholic to abstain from ETOH abuse

high acetaldehyde levels cause unpleasant rxns

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17
Q

BAC is determined by the __ of ETOH ingestion

A

rate

0.08 by 2-4 drinks/hr

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18
Q

12 oz beer = one drink = ___ liquor = ______ wine

A

1.5 oz liquor

5 oz wine

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19
Q

ETOH MOA

A

1) potentiates effects of GABA at GABAa receptors (hyperpolarization)
2) inhibits glutamate-activated NMDA receptors –> ETOH related memory loss

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20
Q

describe wernicke-korsakoff syndrome

A

aka wet brain or alcoholic encephalopathy

neurological condition associated with thiamine deficiency B1 in combination with excessive ETOH intake

observe: ocular disturbances, changes in mental state, memory impairment, and movement difficulties

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21
Q

describe fetal alcohol syndrome

A

ETOH is powerful teratogen –> mental retardation, hyperactivity and antisocial behavior

no safe level of alcohol intake for preggers

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22
Q

long-term ETOH consumption affect the following organs

A
  • liver cirrhosis
  • cardiovascular HTN, arrhythmias, etc
  • inhibits ADH in kidney
  • gastritis, cancer in GI tract, ulcers
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23
Q

most common two-drug combination that results in drug-related death

A

cocaethylene = cocaine + ETOH

produced in liver –> intensifies cocaine’s euphoric effects

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24
Q

what should be given to avoid wernicke-kosakoff syndrome

A

thiamine

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25
Q

why give naltrexone for chronic alcoholism?

A

opioid antagonist that blocks reinforcing properties of ETOH and reduces the rate of relapse

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26
Q

flunitrazepam =

A

date rape drug, benzodiazepine

“roofie”

tastesless when dissolve din a beverage, retrograde amnesia

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27
Q

benzodiazepine receptor antagonist useful in treatment of overdose and in reversing the effects of long-acting benzodiazepines used in anesthesia

A

flumazenil

28
Q

MOA benzodiazepines and barbiturates

A

positive modulators of GABAa chloride channels —> increase inhibition

29
Q

how do benzodiazepines and barbiturates work in the reward pathway?

A

activation of GABAa receptors on interneurons leads to decreased activity and reduced release of GABA –> disinhibiton of VTA DA neurons and activation of mesolimbic reward pathway

30
Q

MOA GHB

A

disinhibiton of DA neurons in VTA via GABAb receptors

31
Q

GHB causes…

A 
euphoria
enhanced sensory perceptoion
sedation
felling of social closeness
amnesia "date rape drug"
32
Q

RR of addiction for psychostimulants

A

5

33
Q

“speedballing”

A

IV heroin and cocaine mixed together

34
Q

reward effects of cocaine

A

increased DA release in the nucleus accumbers

35
Q

cocaine produces these effects:

A

intense euphoric effect
increased energy and libido

also linked to cardiovascular toxicity!

36
Q

strongest psychological dependence of any drug

A

cocaine

37
Q

why might you prefer meth over cocaine?

A

price

and effects last 6-24 hrs compared to 20-30min with cocaine

38
Q

amphetamines lead to…

A

euphoria
increased arousal
reduced sleep

39
Q

common name for methylphenidate

A

ritalin

40
Q

“ecstasy” =

A

MDMA

evokes feeling of intimacy and empathy

41
Q

MOA MDMA

A

interferes with 5HT transporters to release 5HT from presynaptic terminals

42
Q

toxicity of MDMA **

A

hyperthermia and dehydration

43
Q

chronic abuse of psychostimulants can lead to ….

A

toxic psychosis that is indistinguishable from paranoid schizophrenia

must be treated with antipsychotic agents (haloperidol or chlorpromazine)

44
Q

RR of addiction for psychedelics/hallucinogens

A

1

45
Q

lysergic acid diethylamide

A

LSD

46
Q

psilocybin =

A

magic mushroom

47
Q

ketamine =

A

special K

48
Q

phencyclidine =

A

PCP or angel dust

49
Q

MOA for LSD and psilocybin

A

release glutamate in cortex via thalmic excitation

taget 5HT2a receptors

50
Q

is LSD addictive?

A

no

does not stimulate mesolimbic doapmine release —> no dependence or addiction and no withdrawal syndrome

51
Q

what type of anesthetic is ketamine?

A

dissociative (look awake but the pt doesn’t remember anything)

52
Q

MOA ketamine and PCP

A

block NMDA type glutamate receptors; decrease activity of cortex and limbic system

53
Q

RR of addiction for opioids

A

4

54
Q

opiates =

A

morphine
codeine
heroin

55
Q

MOA of opioids

A

1) inhibition of GABAergic neurons vi aactivation of mu-opiod receptors leads to disinhibition of the VTA DA neurons causing euphoria
2) inhibition of VTA DA neurons via activation of kapp-opioid receptors (inhibitory) causes dysphoria

56
Q

used for emergency overdose of opioids

A

naloxone

mu opioid receptor competitive antagonist that reverse the effects of morphine or heroin within minutes

57
Q

opioid abstinence syndrome

A

cessatiion of long-term opiate use leads to withdrawal with dysphoria, nausea and vomiting, lacrimation, flu-like, etc.

subsides within 5 days

58
Q

used to treat opioid withdrawal and opioid addiction

A

methadone

long-acting opioid agonist that has easier withdrawal symptoms

59
Q

mu opioid receptor antagonist used primarily for maintenance therapy

A

naltrexone

60
Q

RR of addiction for cannabinoids

A

2

61
Q

synthetic THC approved for treatment of chronic pain

A

dronabinol

62
Q

MOA THC

A

disinhibits DA neurons in the VTA via pre-synaptic cannabinoid receptors –> euphoria, relaxation and sense of well-being

63
Q

MOA nicotine

A

activation of nicotinic acetylcholine receptors on VTA projection neurons result in DA release in nucleus accumbens and PFC

64
Q

MOA varenicline

A

high affinity nACHR agonist that competes for binding with nicotine

65
Q

which is more addictive: shcedule I or V?

A

schedule I

Pharm Exam 3 (11 decks)

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