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345A > Hallucinogens: PCP and Ketamine 15th > Flashcards

Hallucinogens: PCP and Ketamine 15th Flashcards

1
Q

in what sense are dissociative a Hal

A

it decouples perceptual from sensory; can’t make sense of sensory signals

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2
Q

how are dissociative stimulants

A

induce euphoria and numbing= can turn into panic= stimulant

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3
Q

what causes the amnesia in dissociative

A

if brain can’t make sense of sensory signals it won’t encode it

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4
Q

T: muscle flaccidity

A

catalepsy

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5
Q

what schedule is ketamine

A

1

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6
Q

ketamine is being used in … research

A

schizophrenia due to glutamate connection

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7
Q

T: a synthetic analog of a legally restricted or prohibited drug, devised to circumvent drug laws. (dissociates fall under this)

A

designer drugs

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8
Q

what is the full name for dissociative

A

dissociative anesthetic hallucinogen

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9
Q

what 3 drug classes do dissociates fall under

A

depressants, stimulants and hallucinogens

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10
Q

2 things that make them depressant

A

sedative, pain

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11
Q

dissociative separate … from …

A

perception from sensation

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12
Q

3 general effects of dissociative

A

amnesia, analgesic, catalepsy

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13
Q

what were dissociates destined for

A

surgery (didn’t know side effects)

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14
Q

what schedule are these drugs in US?

A

2 for vet use

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15
Q

PCP and ketamine are the same kind of dissociative Hal but have Dif effect

A

f opposite

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16
Q

what was the similar effect of PCP and ketamine

A

anesthesia

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17
Q

street name for ketamine

A

special K, vitamin K (very dangerous have other meanings) bump, green, super acid

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18
Q

how is ketamine in took 4

A

insufflation, inhalation, injection (medical), oral (assault)

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19
Q

how long does onset take for ingestion vs insufflation, inhalation, injection

A

ingestion: 2 hour

others 10-60 min

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20
Q

full name for PCP

A

phencyclidine

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21
Q

why is PCP less common

A

pricer

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22
Q

street names for PCP

A

Angel Dust, ozone, rocket fuel

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23
Q

what is the ironic thing about the street names of PCP

A

refer to methods of preparation

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24
Q

2 intake methods for PCP how long for onset for each 2

A

insufflation (1min) or inhalation (5 min)

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25
Q

how long does PCP last

A

30 min onset to 18 hours

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26
Q

T: a yellowish “oil” solution that cigarettes or joints are dipped in PCP

A

embalming fluid

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27
Q

T: PCP mixed with Marijuana

A

killer joints (sherms)= rocket fuel best

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28
Q

T: PCP crystals ground and sprinkled on oregano, parsley, alfalfa and smoked

A

angel dust (the oregano doesn’t do anything)

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29
Q

why does dosage influence the MOA on the dissociatives

A

binding affinity of chemical at Dif doses

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30
Q

what NT disrupted in low doses

A

seretonin and dopamine

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31
Q

any permissive hypothesis with dissociative

A

no because it has to do with binding affinity

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32
Q

what do dissociatives do to dopamine of seretonin

A

repuptake inhibitor

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33
Q

what does it do as a reuptake inhibitor

A

disengages the mechanism (messing with metatropic function not just blocking= LT effects)

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34
Q

low doses act as a partial agonist for …2

A

5-HT2A, D2 receptors (reward potential and Hal components)

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35
Q

high doses influence what NT

A

Ach

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36
Q

what do high doses do to ach

A

antagonist

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37
Q

what are the act receptors called 2

A

muscurininc and nicotinic

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38
Q

… NT is responsible for memory

A

ACH

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39
Q

what does antag of nicotinic receptors do

A

muscle contractions

40
Q

what does antag of muscarinic receptors do 3

A

memory deficits, analgesia and arousal

41
Q

what is an NT effected at both low and high doses

A

NMDA (glutamate) receptor

42
Q

what does it do at NMDA

A

antagonize

43
Q

T: lasting strengthening of synaptic connections due to repeated firing

A

LT potentiation

44
Q

what happens to LT potentiation on dissociative

A

disrupts it with stopper signal due to lack of NMDA = fire apart wire apart= decouple

45
Q

what is the behaviour effect of LT potentiation disruption

A

results in disordered learning from not being able to remember

46
Q

the Moa depends on dose but do the effects?

A

yes Dose dependant effects

47
Q

how much is a low dose

A

under 5 mg

48
Q

effects of low dose of PCP and ketamine ? 2

A

drunk-like state, numbness in extremities

49
Q

at what dose does it work like an anesthetic

A

low

50
Q

what is a moderate dose

A

5-10 mg

51
Q

effects at moderate dose

A

disconnectedness from environment, dissociativeness from body/body distortion (feels like being low in iron)

52
Q

high dose effects?

A

sympathomimetic, hallucinations (distortions)

53
Q

is it true sympathy mimetic?

A

no its panic in response to reaction to what’s happening to your body

54
Q

for people who use high doses what are the lingering effects

A

up to 2 moths of Lingering schizophrenic-like symptoms

55
Q

T: looking at something and can only see one part of picture e.g persons eye

A

microscopia

56
Q

what is macroscopia

A

can’t focus on anything see everything (attention)

57
Q

delusions, paranoia, disordered thinking, catalepsies and catatonia, sparse/garbled speech, micro/macroscopia occur from high doses of PCP or ketamine what do these resemble

A

schizophrenia

58
Q

what does this tell us about schiz

A

support glutamate hypothesis (instead of dopamine)

59
Q

Ketamine: “…” perceive experience simulating near-death (heading toward light) or only being able to see apart of setting

A

keyhole

60
Q

what dose causes depressant effects

A

moderate

61
Q

Analgesia means less exertion

A

f allows for excessive exertion

62
Q

problem with Analgesia allows for excessive exertion

A

injury to self

63
Q

what does it feel like to be on ketamine or PCP: why?

A

“Superhuman” strength and “invulnerability” because not feeling pain= not getting feedback from body

64
Q

T: Delusional fantasies of omnipotence, power, perception

and the belief in a “god-like” status effect of ketamine

A

megalomania

65
Q

how does ketamine change fear of death

A

pathological decreased fear of death

66
Q

illogical fear of death with megalomania in ketamine or PCP

A

no for PCP (say god but won’t follow through e.g. flying)

ketamine will follow through

67
Q

what happens to megalomania LT

A

perception stays LT from chronic prolonged use

68
Q

PCP and ketamine results in depressive symptoms

A

depressive- like symptoms (drug induced Dif course)

69
Q

is the depression caused long term?

A

morphs into schizo like psychosis

70
Q

what causes the depressive symptoms from PCP and ketamine

A

Chronic antagonism of glutamate receptors leads to deficits in memory, speech, logic

71
Q

is there tolerance with PCP and ketamine?

A

accrued tolerance

72
Q

what does LT depression mean

A

neurons not connected dendrites pulling back= strictly physiological not emotional

73
Q

what is accrued tolerance

A

increasing amounts over time as you keep taking more

74
Q

why do they separate animal surgeries using dissociates

A

to avoid accrued tolerance= Separation of administration by days prevents tolerance

75
Q

how does tolerance influence drug behaviour for users

A

Prolonged regular intake requires higher doses to achieve effect

76
Q

is there tolerance to psychedelic effects?

A

Chronic ketamine injection results in permanent tolerance to psychedelic effects (NMDA receptors so down regulated)

77
Q

is there physical dependance with dissociatives

A

only for PCP

78
Q

does PCP cause brain damage

A

hard to say because its associated with a lifestyle

79
Q

what causes the dependance in PCP

A

effects on dopaminergic centers

80
Q

is the withdrawl of PCP the result of brain damage

A

maybe

81
Q

is there psychological dpeednace in dissociatives

A

yes

82
Q

what psycholigcal depednace symptoms

A

cravings have been observed, related to euphoria

83
Q

how has ketamine been used therepudically

A

to treat depression

84
Q

T: ketamine used to treat depression

A

ketamine psychedelic therapy

85
Q

there is a close relationship between glutamate and … in brain

A

glucocorticoids (glutamate activating cortisol in brain= too much surpasses seretonin)

86
Q

what is the logic behind using ketamine for treating depression

A

target antagonize glutamate receptors on glucocorticoid receptors

87
Q

target antagonize glutamate receptors on glucocorticoid receptors did studies find this to be true with MDD?

A

one dose of Ketmaine resulted in alleviation of depressive symptoms within hours

88
Q

how long did the effects of ketamine on dep last

A

lasted a week

89
Q

what happened to suicidal ideation after ketamine

A

Suicidal ideation diminished in 40 min (better than antidepressants in this way)

90
Q

T: Inhibition of glutamate at NMDA allows for glutamate to bind elsewhere, and facilitate BDNF

A

glucocorticoid theory

91
Q

what happens if brain is saturated in cortisol

A

LT fight flight changes = anxiety

92
Q

what does cortisol do to seretonin system

A

antagonists it

93
Q

what does cortisol do to seretonin system

A

antagonists it

94
Q

MDD has higher levels of glucocorticoids

A

t

95
Q

free floating cortisol will cause worse MDD

A

f no whee to sit in NMDA remove self from glucocorticoid= seretonin back into play on receptors

96
Q

ketamine provides support for what theory of depression brain chemistry

A

Glucocoritcoid theory not BDNF

345A (20 decks)

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