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
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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
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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
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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)
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5
Q

naturally occurring stimulants

A
  • cocaine
  • ephedrine
  • cathinone
  • methcathinone
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6
Q

synthetic stimulants

A
  • amphetamines (adderall)
  • methamphetamines (crystal meth)
  • methylphenidate (ritalin)
  • pipradrol (treat obesity)
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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
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8
Q

Fair Sentencing Act 2010

A
  • eliminated minimum sentence requirement for small amount of crack
  • Obama Administration
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9
Q

Comprehensive Methamphetamine Control Act 1996

A
  • increased penalties for meth manufacturing & trafficking
  • caused manufacturing to move outside US but still imported
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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
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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
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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
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13
Q

freebase cocaine

A
  • mixed with ether (flammable) to break down hydrochloride
  • heated to vaporize
  • inhale vapor
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14
Q

crack cocaine

A
  • mixed with baking soda & water to form crystals
  • vaporized & inhaled
  • name comes from cracking sound of baking soda heated
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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
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16
Q

major metabolite stimulants

A
  • benzoylecgonine
  • small amount of drug metabolized to an active compound norcocaine
  • norcocaine target of drug testing
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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