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PSYC383 - Psychopharmacology > Cocaine & Amphetamines > Flashcards

Cocaine & Amphetamines Flashcards

1
Q

routes of administration for cocaine

A

ingested
injected - dissolve with water, better high than snorting and no numb. QUICKLY GOES AWAY
snorted - most popular: rapid onset and facial/nose numbness… numbness>euphoria
smoking crack
applied topically

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2
Q

duration of effect for cocaine powder

A

1-3 hrs

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3
Q

duration of effect for cocaine crack

A

5-30 minutes

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4
Q

duration of effect for cocaine amph

A

2-12 hours

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5
Q

NT directly affected by cocaine

A

dopamine, norepinephrine, and serotonin

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6
Q

how is the tolerance of cocaine

A

moderate
with some reverse tolerance

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7
Q

how is the physical dependance vs psychological dependence of cocaine

A

phys = moderate
psyc = high

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8
Q

what are the withdrawal symptoms from cocaine

A

depression, anxiety, drug craving, and binging (can lead to an acute tolerance)

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9
Q

what schedule is cocaine under

A

1

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10
Q

what kind of a stimulant is cocaine

A

psychomotor stimulant

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11
Q

cultural use of cocaine

A

was found in coca leaves growing in south america: chewed up.. slower onset but better endurance and alertness

  • coca leaves were an important in inca culture: religious ceremonies and currency
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12
Q

where in SA was cocaine found

A

mostly columbia, then peru and then bolivia

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13
Q

freuds use of cocaine: 1850s

A

he was an early advocate for it: depression, fatigue, indigestion, asthma, syphilis, autism, morphine addiction and alcoholism
- eventually opposed it

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14
Q

medicinal use of cocaine

A

“medical miracle”
- used as an anesthetic
- patented tonics and elixirs (coca cola in 1880)
- treatment for depression and morphine dependence

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15
Q

harrison narcotic act

A

prohibited coke being sold OTC in 1916
- allowed govt to track users and tax opium/heroin/cocaine

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16
Q

past recreational use of cocaine

A

1970/1980: cocaine use by snorting or IV injection increased due to rock bands popularity (edgy and cool)
1984: crack cocaine started
mid 1980s: US established harsh penalties for possession/distribution since crack cocaine started to get really popular

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17
Q

why was cocaine not initially seen as addictive

A

phys withdrawal symptoms were not as bad

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18
Q

modern day use of cocaine

A

coke is the 3rd highest drug used in Canada via the general population (15+)
- 1st is alc (78%), 2nd is weed (14.8%)

upward trend in coke use since 2013

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19
Q

how much of the general pop used coke in the past year

A

2.5%

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20
Q

current canadian penalties for coke

A

unlawful possession = fine up to $1000 or 6 months imprisonment
- bigger penalties for bigger quantities
- driving while impaired is a criminal offence

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21
Q

BC decriminalization pilot program

A

jan23-jan26
adults with less than 2.5g of CERTAIN illegal drugs arent subject to arrest or criminal charges and drugs are NOT seized

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22
Q

UNODC report on cocaine

A

united nations office on drugs and crime
- global estimate of cocaine use is 0.37%
- AUS = 2.5%
- USA = 2.4%
- UK = 2.3%
- CAN = 2.5%

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23
Q

coca leaf type of cocaine

A

natural, taken orally, has very little abuse potential

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24
Q

coca paste type of cocaine

A

from cocaine sulfate, smoked

25
crack type of cocaine
freebase cocaine dissolved in baking soda - converted from cocaine HCl smoked, gives a faster and more intense high *crack is less flammable than freebase
26
cocaine type of cocaine
comes from cocaine hydrochloride (isolated from leaves) snorted, cannot be smoked since it breaks down at high temps
27
basic pharmacology of cocaine
- cocaine extracted from coca leaves is converted to HCl salt and crystallized - can be turned back into smokeable cocaine via freebasing (crack)
28
how to take cocaine HCl
it is water soluble therefor can be taken orally, intranasally, or IV injection - cannot be smoked
29
cocaine HCl vs freebase (SR BOTD)
HCl - isolated from coca leaves - taken topically, via injection, orally, insufflation - 70-75% bioavailability from snorting - 10-30sec onset from snorting - 10 min for peak brain levels from snorting - 2 hour duration of action crack - converted from cocaine HCl via baking soda - inhaled aka smoking - 90% bioavailability from smoking - 1-2 sec onset from smoking - 8 sec for peak brain level from smoking - 5-15min duration of action
30
cocaine absorption: IV injection and smoking VS snorting and oral use
IV injection and smoking = extremely fast absorption snorting and oral use = slow absorption
31
why does cocaine quickly distribute through the body
because it is water and fat soluble and is able to pass through BBB rapidly *can also pass through placenta
32
how is cocaine metabolised
via the cytochrome P450 enzymes in liver - there is individual variation in uptake and metabolism of cocaine
33
cocaine half life vs major metabolites half life
c: 0.5-1.5hr mm: 8ish hours
34
cocaine elimination
Excreted in the urine (mainly) - detectable for up to 3 days sweat saliva/blood - detectable for up to 2 days breast milk *metabolites are detectable in chronic users for up to 2 weeks
35
what factors affect cocaine in the system
weight frequency dosage persons metabolism
36
which receptors does cocaine block and how
DA, NE, 5-HT: by inhibiting their membrane transporters
37
which pathway is critical for the behavioral effects of psychostimulants
DA pathway - mesolimbic DA system plays a role in reinforcement and motivational mechanisms
38
which ion channels does cocaine inhibit and how
inhibits voltage gated Na channels = blocks nerve conduction - applied locally this acts as a local anesthetic
39
which anesthetics were developed from cocaine
procaine aka novocaine and lidocaine aka xylocaine
40
animal study for cocaine and mice
genetically modified mice w a functional dopamine transporter that is INSENSITIVE to cocaine, fail to self admin the drug - DATki mice:
41
rats and cocaine: correlation of behavioral responses and individual differences in neurochemistry
Rats that were naturally high cocaine responders (HCR) showed strong locomotor responses in the open field (compared to LCR or control aka saline) *around 90 min mark, HCR rats differed significantly from control and LCR
42
why were LCR rats able to clear out DA more effectively than HCR
LCR have greater baseline DAT expression and were able to clear DA in the NAcc and dorsal striatum more effectively
43
mechanism of cocaine (human studies) - what is used to study this
PET imaging is used to estimate DAT occupancy
44
what does the intensity of the high depend on?
the amount of DAT occupancy AND the rate at which occupancy occurs (e.g., smoking will cause rapid occupancy)
45
Sympathomimetic drugs produce?
symptoms of sympathetic nervous system activation
46
ST effects of Sympathomimetic drugs
Constricted blood vessels, dilated pupils, increased body temperature, increased BP… Feeling of euphoria, exhilaration, well-being Increased wakefulness and alertness Enhanced self-esteem, self-confidenct
47
effects of cocaine as dose increases
Bizarre, erratic, violent behavior is possible Restlessness, irritability, anxiety, panic, paranoia Tremors, muscle twitches High doses can be fatal (seizures, stroke, heart failure...)
48
effects of extreme use of cocaine
heart problems, seizures, death and addiction
49
unusual side effect of cocaine use
formication: delusional parasitosis - a delusion that insects are crawling in and under one’s skin
50
LT effects of cocaine use
Cardiovascular effects Seizures Sexual dysfunction Risk to nasal cavities if snorting Risk to lungs if smoking Risk of injury or infections from cracked pipes
51
when are the severe effects of cocaine most likely
with high dosages and in chronic users
52
cocaine dependence and misuse
most people who try it dont progress to misuse BUT for those that do: use escalates, binges are more common, ROA can switch from snorting to crack or IV injection
53
cocaine tolerance and withdrawal symptoms
acute tolerance - WD symptoms: phys symptoms are not life threatening but psych symptoms are compelling
54
for cocaine tolerance/sensitization, what do we consider?
pattern of drug exposure, time since last dose, response being measured E.g., tolerance to locomotor-stimulating effects; sensitization to stereotyped behaviours
55
chronic cocaine use: Molecular adaptations in NAcc include
decreased DA synthesis decreased DA release less DAT binding less D2/D3 receptor binding
56
cocaine dependency causes..
cognitive deficits: impulse control, issues with working memory, decision making, etc.
57
brain parts affected by chronic cocaine use
inferior frontal AND temporal gyrus, insula, anterior cingulate gyrus, thalamus, dorsal striatum
58
effects of chronic cocaine use
regular high dose use: - strokes, seizures, perforation of nasal septum if its snorted - panic attacks, paranoid psychosis

PSYC383 - Psychopharmacology (3 decks)

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