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PHAR 230 > M5 L2: CNS Stimulants and Drugs of Abuse > Flashcards

M5 L2: CNS Stimulants and Drugs of Abuse Flashcards

1
Q

physical dependence

A

dependence involving emotional-motivational withdrawal sympt (ex: dysphoria, anhedonia)

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2
Q

physical (physiologic) dependence

A

dependence involving persistent physical-somatic withdrawal sympt

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3
Q

all addictive drugs activate the…

A

mesolimbic system = reward pathway

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4
Q

what are ex of stimulants

A

amphetamines, cocaine, xanthines and nicotine

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5
Q

what are ex of depressants

A

opioids, alcohol, barbiturates, benzodiazepines, GHB

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6
Q

ex of anti-depressants

A

SSRI, SNRI, MAOI

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7
Q

ex of anti-psychotics

A

typical and atypical

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8
Q

what has its own classification for drugs of abuse

A

cannibis

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9
Q

what are ex of inhalants

A

nitrous oxide, ketones, hydrocarbons

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10
Q

what are 2 non-addictive drugs of abuse

A
  • hallucinogens
  • dissociative anaesthetics (NMBAR antagonists)
    (they don’t target the mesolimbic sys!)
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11
Q

examples of hallucinogens

A

lysergic acid diethylamide (LSD) - mescaline - psilocybin

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12
Q

ex of dissociative anaesthetics (NMDAR antagonists)

A

phencyclidine (PCP) - ketamine

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13
Q

what are amphetamines

A
  • alpha-methylphenethylamine
  • synthetic sympathomimetics
  • derivatives: amphetamine, methamphetamine
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14
Q

what is the mech of action for amphetamines

A
  • increase DA release through: competitive decrease of DA transport back to the presynaptic neuron, and decreased VMAT -> decreased DA reuptake by synaptic vesicles
  • increased NE release (sympathomimetic action)
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15
Q

what are amphetamines

A

weak base (oral bioavailability varies w GI pH

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16
Q

what is the half life of amphetamines

A

relatively short (9-14h)

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17
Q

what is the metabolism of amphetamines

A

in the liver - hydroxylation, deamination, conjugation

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18
Q

how are amphetamines excreted

A

in urine - 30-40% unmetabolized

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19
Q

how are amphetamines administered

A

oral, smoked, IV

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20
Q

what are the effects of amphetamines

A
  • euphoria and excitement
  • cognitive enhancement
  • anorexia
  • increased motor activity
  • fatigue resistance
  • improved performance of tedious, repetitive tasks
  • sympathomimetic actions* ex: vasoconstriction, increased bp, tachycardia, decreased motility
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21
Q

what are amphetamines CVS adverse effects

A

dysrhythmias, hypertension, raynaud’s phenomenon

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22
Q

what are amphetamines CNS adverse effects

A

tremors, agitation, confusion

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23
Q

what are amphetamines respiratory adverse effects

A

tachypnea

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24
Q

what are amphetamines GI adverse effects

A

anorexia, weight loss

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25
Q

what are amphetamines urinary adverse effects

A

dysuria, retention

26
Q

what are amphetamines eye adverse effects

A

mydriasis, blurred vision

27
Q

what are the overall adverse effect of amphetamines

A
  • SNS stim
  • tolerance, addiction, dependence
28
Q

indications of amphetamines

A
  • ADHD
  • narcolepsy
  • obesity
29
Q

contraindications of amphetamines

A
  • CVS disease
  • anxiety and agitation
  • history of drug abuse
30
Q

what is MDMA (ecstasy-molly)

A

3,4-Methylenedioxymethamphetamine
- amphetamine-related compound
- was used in psychotherapy - not, only recreational

31
Q

what is the mech of action for MDMA (ecstasy-molly)

A
  • as amphetamines
  • high affinity to serotonin transporter -> increased serotonin reuptake and concentration
  • prolonged use causes serotonin depletion
32
Q

what are the effects of MDMA (ecstasy-molly)

A
  • increased empathy, euphoria, and heightened sensations
  • hyperthermia** from dehydration, tachycardia, hallucinations, panic attacks, agitation
33
Q

what is cocaine

A

coke!
- alkaloid isolated from Erythroxylum coca leaves
- strong stim
- was used as: local anaesthetic, mydriatic

34
Q

what is the mech action of cocaine

A
  • cocaine inhibits the reuptake of dopamine (DA) by blocking the dopamine transporter (DAT), leading to an increase in extracellular dopamine concentration
  • cocaine also inhibits the reuptake of NE by blocking the NE transporter, resulting in an increase in extracellular concentration
35
Q

where is cocaine absorbed

A

lungs and GI (stomach)

36
Q

where is cocaine distributed to

A

rapidly into the brain

37
Q

how is cocaine metabolized and where

A

by cholinesterase enzymes (liver and plasma)

38
Q

half time of cocaine

A

short (1hr)

39
Q

how is cocaine excreted

A

in urine

40
Q

how is cocaine administered

A

snorting (salt powder), smoke inhalation (crack cocaine), IV (solution), topical (solution)

41
Q

what are the effects of cocaine

A
  • euphoria + excitement
  • cognitive enhancement
  • anorexia
  • increased motor activity
  • fatigue resistance
  • peripheral sympathomimetic actions
42
Q

CVS adverse effects of cocaine

A

dysrhythmias, hypertension, CAD

43
Q

CNS adverse effects of cocaine

A

repeated use:
- tremors, agitation, paranoid delusions, stroke
overdose:
- seizures, hyperthermia, hallucination, coma, death

44
Q

skin adverse effects of cocaine

A

pruritus (itching)

45
Q

respiratory adverse effects of cocaine

A

tachypnea, hemoptysis, bronchospasm, nasal septum atrophy

46
Q

GI adverse effects of cocaine

A

anorexia, dry mouth, gingivitis, dental caries

47
Q

eye adverse effects of cocaine

A

mydriasis, blurred vision

48
Q

can tolerance, addiction, dependence happen w cocaine

A

YES. obvi

49
Q

tolerance to cocaine

A
  • may develop
  • reverse tolerance: sensitivity to small doses
50
Q

addiction to cocaine

A

HIGH - develops after only few exposures

51
Q

dependence to cocaine

A
  • withdrawal sympt: < opioids
  • fatigue, dysphoria, anxiety, irritability, sleepiness, agitation
52
Q

what is LSD

A
  • ergot alkaloid
  • hallucinogen
  • psychotomimetic
  • was used in psychotherapy
  • only recreational

DOES NOT TARGET MESOBOLIC SYS

53
Q

onset of action, duration, typical dose of LSD

A

onset of action: 30 min
duration: 6-12 hrs
typical dose: 25 mcg

54
Q

mech of action in LSD

A

5-HT2a receptor agonist in thalamus, increases glutamate in cortex

55
Q

what are the effects of LSD

A

psychosis-like manifestations:
- depersonalization, hallucinations, distorted time perception
somatic manifestations:
- dizziness, nausea, paresthesia, blurred vision, could cause abortion
- rapid tolerance
- no addiction or dependence

56
Q

sources of cannabinoids

A
  1. endogenous
    ex: 2-arachidonyl glycerol (2-AG)
  2. exogenous
    - plants: cannabis (marijuana)
    - synthetic: chemical substances
57
Q

what is the main psychoactive constituent of cannabis

A

Δ ^9 -tetrahydrocannabinol (THC) is the primary psychoactive compound in cannabis.

58
Q

what is the mech of action of cannabinoids

A
  • activation of cannabinoid-1 receptors leads to an increase in presynaptic GABA neurons in the ventral tegmental area, resulting in the disinhibition of dopamine neurons
59
Q

how are cannabinoids
absorbed:
onset of action:
peak:
half life:

A

absorbed: resp sys
onset of action: few min
peak: 1-2 hrs
half life: 4 hrs

60
Q

CNS effects of cannabinoids

A
  • euphoria, relaxation, sense of well being, and grandiosity
    – Disorientation to time & space
    – Visual distortion, drowsiness, diminished coordination
    – Psychotomimetic, depressant effect & pain relief

can also cause: Tachycardia, vasodilation & bronchodilation

61
Q

addiction and dependence of cannabinoids

A

Relatively low risk of addiction
* Withdrawal symptoms:
– Mild & short-lived
– Restlessness, irritability, mild agitation, insomnia, nausea,
cramps

PHAR 230 (31 decks)

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