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

M5 L2: CNS Stimulants and Drugs of Abuse Flashcards

(61 cards)

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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
what are amphetamines urinary adverse effects
dysuria, retention
26
what are amphetamines eye adverse effects
mydriasis, blurred vision
27
what are the overall adverse effect of amphetamines
- SNS stim - tolerance, addiction, dependence
28
indications of amphetamines
- ADHD - narcolepsy - obesity
29
contraindications of amphetamines
- CVS disease - anxiety and agitation - history of drug abuse
30
what is MDMA (ecstasy-molly)
3,4-Methylenedioxymethamphetamine - amphetamine-related compound - was used in psychotherapy - not, only recreational
31
what is the mech of action for MDMA (ecstasy-molly)
- as amphetamines - high affinity to serotonin transporter -> increased serotonin reuptake and concentration - prolonged use causes serotonin depletion
32
what are the effects of MDMA (ecstasy-molly)
- increased empathy, euphoria, and heightened sensations - hyperthermia** from dehydration, tachycardia, hallucinations, panic attacks, agitation
33
what is cocaine
coke! - alkaloid isolated from Erythroxylum coca leaves - strong stim - was used as: local anaesthetic, mydriatic
34
what is the mech action of cocaine
- 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
where is cocaine absorbed
lungs and GI (stomach)
36
where is cocaine distributed to
rapidly into the brain
37
how is cocaine metabolized and where
by cholinesterase enzymes (liver and plasma)
38
half time of cocaine
short (1hr)
39
how is cocaine excreted
in urine
40
how is cocaine administered
snorting (salt powder), smoke inhalation (crack cocaine), IV (solution), topical (solution)
41
what are the effects of cocaine
- euphoria + excitement - cognitive enhancement - anorexia - increased motor activity - fatigue resistance - peripheral sympathomimetic actions
42
CVS adverse effects of cocaine
dysrhythmias, hypertension, CAD
43
CNS adverse effects of cocaine
repeated use: - tremors, agitation, paranoid delusions, stroke overdose: - seizures, hyperthermia, hallucination, coma, death
44
skin adverse effects of cocaine
pruritus (itching)
45
respiratory adverse effects of cocaine
tachypnea, hemoptysis, bronchospasm, nasal septum atrophy
46
GI adverse effects of cocaine
anorexia, dry mouth, gingivitis, dental caries
47
eye adverse effects of cocaine
mydriasis, blurred vision
48
can tolerance, addiction, dependence happen w cocaine
YES. obvi
49
tolerance to cocaine
- may develop - reverse tolerance: sensitivity to small doses
50
addiction to cocaine
HIGH - develops after only few exposures
51
dependence to cocaine
- withdrawal sympt: < opioids - fatigue, dysphoria, anxiety, irritability, sleepiness, agitation
52
what is LSD
- ergot alkaloid - hallucinogen - psychotomimetic - was used in psychotherapy - only recreational DOES NOT TARGET MESOBOLIC SYS
53
onset of action, duration, typical dose of LSD
onset of action: 30 min duration: 6-12 hrs typical dose: 25 mcg
54
mech of action in LSD
5-HT2a receptor agonist in thalamus, increases glutamate in cortex
55
what are the effects of LSD
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
sources of cannabinoids
1. endogenous ex: 2-arachidonyl glycerol (2-AG) 2. exogenous - plants: cannabis (marijuana) - synthetic: chemical substances
57
what is the main psychoactive constituent of cannabis
Δ ^9 -tetrahydrocannabinol (THC) is the primary psychoactive compound in cannabis.
58
what is the mech of action of cannabinoids
- 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
how are cannabinoids absorbed: onset of action: peak: half life:
absorbed: resp sys onset of action: few min peak: 1-2 hrs half life: 4 hrs
60
CNS effects of cannabinoids
- 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
addiction and dependence of cannabinoids
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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