STIMULANTS Flashcards
1
Q
cocaine history
*Erythroxylum coca
A
- chewed leaves to provide energy starting 16th century
- not isolated til 1850s → higher concentration
- coca = chewed
2
Q
isolated cocaine
A
- increase in purity & concentrated
- POTENT
- snorted, injected, inhaled, rubbed on gums
- fast PK vs. chewing coca
- treatment for asthma, depression, indigestion
- local anesthetic
3
Q
cocaine use over years
A
- coca-cola had 60mg of cocaine
- 1914 Harrison Act limited cocaine in products
- 1920-1930s use declined in favor of amphetamines
- increase in 1960s and peaked in 1980s
4
Q
amphetamines
A
- synthetic stimulants
- prescribed for colds, obesity, narcolepsy, ADHD
- addiction rates rose → was used as treatment for heroin misuse
- speed freaks (opiates & stimulants)
5
Q
naturally occurring stimulants
A
- cocaine
- ephedrine
- cathinone
- methcathinone
6
Q
synthetic stimulants
A
- amphetamines (adderall)
- methamphetamines (crystal meth)
- methylphenidate (ritalin)
- pipradrol (treat obesity)
7
Q
Anti-Drug Abuse Acts
‘86 and ‘88
A
- specified penalties for sales & possession
- set limits on legal amount
- higher penalty for crack possession vs. cocaine
- Black people heavily targeted
8
Q
Fair Sentencing Act 2010
A
- eliminated minimum sentence requirement for small amount of crack
- Obama Administration
9
Q
Comprehensive Methamphetamine Control Act 1996
A
- increased penalties for meth manufacturing & trafficking
- caused manufacturing to move outside US but still imported
10
Q
Combat Methamphetamine Epidemic Act 2006
A
- regulate sales of products containing pseudoephedrine or things used to make meth
- causes production to return to Mexico
11
Q
cocaine sulfate
A
- smokable
- plant is processed by mashing & soaking (sulfuric acid)
- processed into a paste, then hung to dry
- creates smokable form; placed at cigarette end or mixed with tobacco
12
Q
cocaine hydrochloride
street cocaine
A
- powder form
- converted from leaves paste to powder by adding various chemicals & drying
- snorted, injected, oral or topical
13
Q
freebase cocaine
A
- mixed with ether (flammable) to break down hydrochloride
- heated to vaporize
- inhale vapor
14
Q
crack cocaine
A
- mixed with baking soda & water to form crystals
- vaporized & inhaled
- name comes from cracking sound of baking soda heated
15
Q
duration cocaine vs. amphetamines
A
- cocaine short-lasting (20-80mins)
- amphetamines long-lasting (4-12hrs)
- different formulation & administration
- metabolites both eliminated after 5 days
16
Q
major metabolite stimulants
A
- benzoylecgonine
- small amount of drug metabolized to an active compound norcocaine
- norcocaine target of drug testing
17
Q
PD route of action
A
- intra-nasally = 10-15min
- IV & smoking = fastest administration, matter of seconds
18
Q
cocaine on PNS
peripheral nervous system
A
- potent local anesthetic effects
- can test purity by rubbing on gums (numbness)
- powerful constrictor of vessels
- not commonly used for surgery → high misuse potential
- use derivatives instead
19
Q
cocaine on CNS
A
- powerful psychostimulant with strong reinforcing qualities (behavioral)
- increases synaptic actions of dopamine, norepinephrine, and serotonin (physiologically)
20
Q
how can a drug increase synaptic actions of a NT?
A
- blocks reuptake → increase action of NT
- agonist → acts directly at receptor & magnifies NT
- act on autoreceptor → change amount of NT released
- interupting metabolic process → prevent enzymes from breaking drug down
21
Q
COCAINE neutrotransmission & PD
A
- actively blocks transporter reuptake of dopamine, norepinehprhine, & serotonin
- monoamines remain in synaptic cleft → continues binding to receptors
- continued binding → mechanism stays stimulated
- reward pathway continually activating = reinforcement
22
Q
AMPHETAMINE neurotransmission & PD
A
- blocks AND reverses transporter reuptake of dopamine, norepinenphrine, serotonin
- blocks enzymes that degrade monoamines → blocks monoamine oxidase (MAO) in presyn.
- blocks transporter that fills vesicles with monoamines
- high concentration of NT in synaptic cleft for long time
23
Q
positive effects of stimulants
A
- mimicking of sympathetic system
- increased attention related arousal
- improved performance on tasks of vigilance & alertness
- increased sense of self-confidence & well-being
- higher doses → euphoria, then desire for drug
- prolonged, intense orgasms if taken prior to sex
24
Q
sympathomimetic
A
- effects that mimic sympathetic nervous system
- positively reinforcing
- enjoyable feeling from stimulants
25
Q
negative effects of stimulants
A
- appetite suppressant
- sleep prevention
- irritability
- involuntary motor activity
- arrhythmias
- sensation of bugs crawling on skin
- visual disturbances
- repetitive behaviors
- stimulant psychosis
- overdose
- seizures
- depression
26
Q
stimulant psychosis
A
- paranoid delusions
- similar to paranoid schizophrenia
- side effects of prolonged stimulant use
- can be treated with drugs for schizophrenia
27
Q
chronic use effects
A
- paranoia
- psychotic behavior
- interpersonal conflicts
- comorbidity with psychiatric syndrome
- increased bizarre/violent behavior
- problems with other drugs of misuse
- hallucinations
28
Q
mood effects of stimulants
A
- affect mood both in session & long-term effects
- initial increase in mood
- once metabolized, mood decreases & crashes LOWER than mood prior
- crashes stronger with multiple administrations in a session
29
Q
tolerance & withdrawal
A
- gain tolerance to euphoric feeling
- results in chasing that first high that can’t be reached
- acute tolerance forms with multiple doses per session
- intermittent use contributes to withdrawal
- major treatment problem = helping patients resist urge to start compulsive cocaine use
30
Q
sensitization
A
- consistently found in cocaine/stimulant studies
- reverse tolerance → facilitates system to make effect easier to reach in future
- intermittent use
- repeated exposure to same dose increases response over time
- strong response when seeking, even before administration
- anticipation of reward
31
Q
intermittent use
A
- taking breaks after binging
- contributor to withdrawal
- dysphoria, depression, sleepiness, fatigue, bradycardia
- profound craving
32
Q
nondependent positive reinforcing effects
A
- dopamine in VTA sent to striatum (NAC)
- neurons increase fire when given positively reinforcing stimulus (drug)
- neurons release dopamine to NAC to stimulate activity
33
Q
dependent positive reinforcing effects
A
- dopamine in VTA sent to striatum (NAC)
- activity increases at level of presyn. terminal
- positive reinforcement suppressed due to neuroadaptations
- leads to taking more of drug to reinstate positive reinforcement & silences negative reinforcement
- vicious cycle of dependence
34
Q
nondependent negative reinforcing effects
A
- other brain structures responsible for negative effects/reinforcement
- neg. reinforcement of dysphoria, stress
- norepinephrine system
- **not overly active **
35
Q
dependent negative reinforcing efffects
A
- other brain structures responsible for negative reinforcement
- norepinephrine
- much more active
36
Q
cocaine & alcohol
A
- alcohol combined with cocaine to take edge off effects
- enzymes that metabolize BOTH produce cocaethylene → blocking transporters
- paradoxically increases euphoric effects
- increases risk of dual dependency
- chronic use increases withdrawal
- longer half-life for cocaine
37
Q
cocaine & heroin
A
- speedball
- more common to add cocaine to heroin than vice versa
- enhances pleasurable cocaine effects
- common cause of overdoses → synergistic effects on BP & HR
38
Q
treatment considerations of stimulant misuse
A
- strong reinforcing effects
- high tendency towards relapse
- additional drug dependencies and psychiatric disorders
- immediate abstinence
- primary or secondary addiction
39
Q
types of treatments
A
- 12 step programs
- using psychopharmacology to reduce neg. effects of dependence
- possible drugs = antidepressants, DA receptor blockers, SSRIs, mood stabilizers, anti-seizure meds
40
Q
stimulants to treat ADHD
A
- paradoxical effect (use stimulant to treat hyperactivity?)
- people with ADHD have low levels of dopamine in rewards pathway
- levels are LOWER than optimal levels for brain to function normally
- stimulants block reuptake → more dopamine in synaptic cleft
- increased levels actually brings ADHD levels back to an OPTIMAL LEVEL
41
Q
ADHD drugs
A
- concerta & ritalin → methylphenidate
- adderall → amphetamine
- stattera → non-stimulant & norepinephrine reuptake inhibitor
42
Q
problems with ADHD drugs
A
- side effects can create compliance issues (unpleasant effects → not taking as prescribed)
- strattera associated with teen suicide
- high misuse potential (high prescription rates)
- can be gateway drug to to non-ADHD
