2-hallucinogens Flashcards

1
Q

what class is psilocybin

A

indole hallucinogen

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2
Q

what is the active ingredient in magic mushrooms

A

psilocybin

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3
Q

what are the psychological and physical effects of psilocybin like

A

a mild version of LSD

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4
Q

is it possible to overdose on psilocybin

A

no

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5
Q

where is psilocybin metabolized

A

in the gut

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6
Q

what happens in psilocybin metabolism

A

phosphate groups are removed

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7
Q

what does psilocybin get metabolized into

A

psilocin

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8
Q

what is the mechanism of action of psilocybin

A

5HT2A receptor agonist

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9
Q

what is the mechanism of action of psilocin

A

5HT2A receptor agonist

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10
Q

is psilocybin addictive

A

no

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11
Q

can you get tolerant to psilocybin

A

yes rapidly

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12
Q

what is the structure difference with psilocybin and psilocin

A

psilocybin has an extra phosphate group

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13
Q

where is psilocybin part of religious ceromonies

A

in mexico

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14
Q

what class of drug is DMT

A

an indole

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15
Q

how is DMT usually administered

A

snorted, smoked or injected

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16
Q

why cant DMT be ingested

A

because the gut contains MAO enzyme that destroys it

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17
Q

how long does DMT last + per routes

A

30 mins, regardless of route

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18
Q

what is the mechanism of action of DMT

A

5HT2A, also 5HT2C and 5HT1A agonist + many other receptors

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19
Q

does tolerance happen in DMT + what receptors are involved

A

no tolerance, no decrease in 5HT2A

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20
Q

why is there no tolerane in DMT

A

because less beta arrestin 5HT2A activation

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21
Q

when do natural levels of brain DMT increase in the brain

A

during stress

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22
Q

does DMT occur naturally in the brain

A

yes in mammals

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23
Q

what are the physiological effects of DMT

A

same as LSD and psilocybin (increase BP vasoconstric sweating dilated pupils)

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24
Q

what are the pyschological effects of DMT

A

intense hallucinogenic

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25
Q

what is ayahuasca (Where from)

A

a concoction of plants often brewed as a tea by indigenous people of the Amaxon

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26
Q

what is in ayahuasca

A

2 types of plants, some with DMT and some with beta-carbolines (MAO inhibitors)

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27
Q

what are beta-carbolines

A

MAO inhibitors

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28
Q

why is it good to take DMT with MAO inhibitor

A

DMT wont be degraded in the stomach no more so it can reach the brain

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29
Q

what parts of the brain are activated by ayahuasca

A

parts of the brain involved in vision and memory

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30
Q

what is a pro of ayahuasca

A

it has been used with therapy in withdrawal programs for many drugs

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31
Q

what class is bufotenin

A

indole

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32
Q

where is bufotenin found

A

in the skin of some toads and hallucinogenic plants

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33
Q

what is another name for bufotenin

A

5-hydroxy-DMT

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34
Q

what does bufotenin cause in many users

A

nausea and headache, but some get profound experiences

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35
Q

what is bad about toad toxins

A

they contain cardiac glycosides which can cause fatal heart rhythm to develop

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36
Q

do people produce bufotenin naturally (And who does more)

A

yes, more in schizophrenics maybe

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37
Q

which drug is marketed as an aphrodisiac

A

bufotenin

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38
Q

what is the structural difference of DMT and bufotenin

A

bufotenin has an extra hydroxyl group

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39
Q

what does NPS stand for

A

new psychoactive substances

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40
Q

who invented 2C drugs

A

alexander shulgin

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41
Q

what did alexander shulgin do

A

synthesized a bunch of new psychoactive susbtances and wrote a book about it “PIKHAL_

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42
Q

why are 2C drugs called 2C

A

because of the 2 carbons between the amino group and the benzene ring

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43
Q

what are all 2C drugs (what 2 classes)

A

phenethylamine, a type of catechol

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44
Q

what is the main target of 2C drugs

A

5HT2 receptors (A) and likely other receptors and transporters

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45
Q

what kind of effects do 2C give you (general, 2)

A

combination of hallucinations and stimulation

46
Q

what is the difference with 2C drugs and other psychedelics

A

these ones can kill you

47
Q

what structural change to 2C drugs increase hallucinogenicity

A

bromine or iodine in position 4

48
Q

what happens when you put a bromine or iodine in position 4 in 2C drugs

A

they increase hallucinogenicity

49
Q

how long does benzodifuran (bromo-dragonfly) last

A

1-3 days

50
Q

what is the mechanism of action of benzodifuran (bromo-dragonfly)

A

interacts with 5HT2A and 5HT1 receptors

51
Q

what is the main physiological effect of benzodifuran (bromo-dragonfly) + how

A

vasoconstriction via alpha adrenergic receptor activation

52
Q

how does benzodifuran (bromo-dragonfly) compare to LSD

A

similar but more intense and longer lasting

53
Q

what is bad about benzodifuran (bromo-dragonfly)

A

very narrow window of safe dose

54
Q

have people died with benzodifuran (bromo-dragonfly)

A

yes a lot, very dangerous

55
Q

what class is benzodifuran (bromo-dragonfly)

A

new psychoactive substances - its like a 2C drug

56
Q

what are the symptoms people go to hospital with when taking benzodifuran (bromo-dragonfly)

A

severe agitation, violence, seizures, hyperthermia, excited delirium

57
Q

what class is NBOMe from

A

new psychoactive substances

58
Q

what is the mechanism of action of NBOMe

A

5HT2A full agonist

59
Q

how does NBOMe compare to 2C series in potentcy

A

more potent

60
Q

how potent is NBOMe

A

extremely

61
Q

what is the difference with NBOMe and 2C series

A

2-methoxybenzyl group is added to the 2C backbone

62
Q

what gives the NBOMe drugs such a high affinity

A

the 2-methoxybenzyl group added to the 2C backbone

63
Q

what are the symptoms of NBOMe

A

same as 2-C, deadly

64
Q

what is the difference with benzodifuran (bromo-dragonfly) and 2C series

A

2 furan extra

65
Q

what is the name of the NBOMe series (what does it stand for)

A

N-benzyl-oxy-methyl

66
Q

what are the original deliriants

A

anticholinergics

67
Q

what are anticholinergics like as hallucinogens

A

they can give hallucinogenic effects but they often dont remember them (original deliriants)

68
Q

what are 5 physiological symptoms of anticholinergics

A

increase HR, dry mouth, lack of perspiration, constipation, difficult pee

69
Q

can anticholinergics be fatal and how

A

yes due to rapid HR and overheating and asphyxia

70
Q

does anticholinergics give euphoria

A

no

71
Q

are anticholinergics pleasant

A

generally no

72
Q

what is the mechanism of actin of does anticholinergics

A

prevent ACh from binding to Muscarinic receptors

73
Q

what does the muscarinic acetylcholine generally do

A

parasympathetic rest and digest and secrete

74
Q

what are the 3 major anticholinergics

A

atropine
scopolamine
hyoscyamine (maybe)

75
Q

what are 4 plants that contain anticholinergics

A

deadly nightshade/belladonna
mandrake
hensbane
jimsonweed (Datura)

76
Q

what are PCP and ketamine classified as (2 classifications)

A

dissociative anesthetics and deliriants

77
Q

what is different with PCP and ketamine and other hallucinogens

A

they completely remove you from reality

78
Q

what are 4 bad things liked to PCP and ketamine

A
  • suicides (severe depression)
  • drownings
  • self-inflicted wounds
  • violence
79
Q

how do people administer PCP

A

dip cigarettes into freebase form then smoke (not oral)

you can also snort and inject

80
Q

how long does PCP last

A

4-8 hours

81
Q

how do people administer ketamine

A

usually snort or inject, you can smoke or swallow

82
Q

how long does ketamine last

A

35-40 minutes

83
Q

what are the behavioural effects of ketamine and PCP at low doses

A
  • relax, warm, numb
  • euphoria, floating
  • distorted body image
  • analgesia!!!
  • near death like experiences
  • increase in locomotion in animals
84
Q

why do they speculate that ketamine and PCP can increase DA levels

A

there is an initial increase in locomotion in animals

85
Q

why is ketamine and PCP so different from other hallucinogens

A

because they are anesthetics

86
Q

what are the behavioural effects of PCP at high doses

A
  • psychosis (long lasting)
  • violent paranoia
  • sudden and extreme mood changes
  • stereotypical movements (repeated non-productive movements)
  • catalepsy
87
Q

what is catalepsy

A

rigid body mosture

88
Q

how long can psychosis from PCP last

A

several weeks

89
Q

is PCP or ketamine used at higher doses

A

more often PCP

ketamine isnt usually used at high concentrations

90
Q

what is the mechanism of action of ketamine and PCP

A

block ion channel in NMDA glutamate channel - Ca++ ions cant flow through

91
Q

is ketamine and PCP or cocaine more reinforcing

A

cocaine

92
Q

what NT systems does ketamine and PCP affect

A

wide variety - glutamate, NA, DA, 5HT, ACh

93
Q

are ketamine and PCP reniforcing

A

yes in animals

94
Q

what are the only reinforcing hallucinogens in animals

A

ketamine and PCP

95
Q

does DA cause the reinforcement of ketamine and PCP

A

no

idk why

96
Q

when do most PCP problems occur and why

A

if they enter a psychotic state, they wont feel pain

97
Q

what drug damages the bladder

A

ketamine

98
Q

what does ketamine damage the most and how

A

severe bladder damage, stops cells that line the bladder from growing

99
Q

what are symptoms of ketamine cystitis

A

bloody urin
pain
incontinence

100
Q

what is ketamine cystitis

A

severe bladder damage

101
Q

how do you ingest salvia

A

chewed (absorbed buccally) or smoked (doesnt work if swallowed)

102
Q

what is the main ingredient in salvia

A

salvinorin A

103
Q

what is different about salvinorin A

A

it is the only known hallucinogen not to contain nitrogen so not an alkaloid

104
Q

what is an alkaloid

A

any of a class of nitrogenous organic compounds of plant origin which have pronounced physiological actions on humans

105
Q

is salvinorin A an alkaloid or no

A

no because it has no nitrogen

106
Q

what is the mechanism of action of salvinorin A

A

binds to kappa opioid receptors

107
Q

what is special about salvinorin A and opioid receptors

A

it is the only non-alkaloid known to bind opioid receptors

108
Q

does salvinorin A bind to 5HT2A receptors

A

nope

109
Q

what are the effects of salvinorin A

A

anxiety fear confusion

110
Q

what class is salvinorin A

A

its unique, deliriant-type