exam 2 Flashcards
what are stimulants
substances that increase activity of sympathetic nervous system
most common stimulants (6)
cocaine, crack, amphetamine, methamphetamine, caffeine, nicotine
cocaine prevalence in U.S.
one of world’s largest consumers of cocaine
black people are less likely than white to use powder and equally likely to use crack
coca leaves
cocaine, oral administration
powder cocaine
snorted, crosses BBB more easily
cocaine source
shrub native to Andes mountains
crack cocaine
smoked for quick and intense high
cocaine route of administration affects ____
amount of cocaine absorbed into bloodstream
cocaine speed of entry into brain (fastest to slowest route of administration)
smoked, injected, snorted, orally
cocaine metabolism system
cytochrome P450 system
cocaine mechanism of action
blocks pain pathways
blocks reuptake of dopamine, norepinephrine, and serotonin (these increase)
schedule of cocaine
II, approved for local anesthetic
adverse effects of cocaine
irritability, hostility, fear, restlessness, paranoia, heart attack
acute effects of cocaine
euphoria and increased energy
increased confidence
sweating/chills
increased heart rate
decreased appetite and need for sleep
chronic use of cocaine
tolerance or reverse tolerance, short-lived withdrawal, irritability
cocaine dependence
weak physical dependence but strong psychological dependence, no FDA approved treatments
amphetamine
more popular than cocaine, more potent effects, stimulates CNS by increasing same neurotransmitters
brand names of amphetamine
adderall, ritalin, concerta
methamphetamine
more lipid soluble form of amphetamine, enters brain faster, more addictive
amphetamine route of administration
oral, injection, intranasal, smoked
amphetamine effect duration
12 hours
methamphetamine effect duration
8 hours
amphetamine mechanism of action
increased postsynaptic levels of dopamine, norepinephrine, and serotonin to larger degree than cocaine
small doses effects of amphetamine
increase energy and alertness, reduced appetite
high doses effects of amphetamine
rush, intoxication, psychosis
meth specific effects
disinhibition, hypersexuality (but can decrease function)
difference between effects of cocaine and amphetamine
amphetamine has slower onset and longer duration but closely resemble one another
chronic use of stimulants
loss of neural tissue in prefrontal cortex
other stimulants
cathinone (khat) and bath salts
brain structures involved in effects of cocaine
increased dopamine in basal ganglia, prefrontal cortex, ventral tegmental area, nucleus acumbens
how have drugs laws for cocaine and crack contributed to racial disparities?
disproportionate incarceration rates and higher penalties for crack possession which was more common among blacks than powder cocaine
hallucinogen
drugs that distort perceptions of reality at relatively low doses
hallucinogen schedule
I
but most are physiologically safe and non-addictive
hallucination
experience involving perception of something that may not actually be there
illusion
altered and distorted perceptions, thoughts, feelings, awareness, insights
hallucinogen plants
peyote, salvia, atropa belladonna
fungi hallucinogen
psilocybin and amanita mushrooms
synthetic hallucinogen
LSD, MDMA, PCP, ketamine
psychedelics
alter perceptions while still allowing person to communicate with the present world
indoleamines
similar to serotonin
LSD, psilocybin, DMT, morning glory
phenylethylamines
similar to dopamine and norepinephrine
peyote, MDMA
deliriants
block acetylcholine
atropa belladonna, henbane, mandrake
dissociatives
cause amnesia, sense of detachment from environment
salvia, PCP, ketamine, amanita mushrooms
most psychoactive hallucinogen
LSD, 25 micrograms
orally administered hallucinogens
psilocybin, LSD, MDMA
route of administration of PCP and ketamine
ingested, snorted, smoked, injected
DMT duration
30 mins
ketamine duration
1 hour
peyote duration
5 hours
PCP and psilocybin duration
6 hours
MDMA duration
7 hours
LSD duration
11 hours
psychedelic hallucinogens affect ___
serotonin, brain areas related to sensory processing, emotions, and higher executive processing
MDMA effects
increased serotonin, dopamine, oxytocin
deliriants effects
prevent binding of acetylcholine
acute effects of hallucinogens
hallucinations, altered perceptions of time and reality, euphoria, increased heart rate
3 stages of LSD and psilocybin
sympathetic nervous system is activated – alterations in perceptions and sensations – self-perception change leading to distortions of reality and emotions
MDMA acute effects
sense of empathy and closeness to others, inner peace
more prone to toxic effects on heart, serotonin syndrome, hyperthermia
deliriants acute effects
hallucinations over illusions
affects temp, vision, hydration, bladder
PCP and ketamine acute effects
depend on dose and environment, high doses can be toxic
schedule I hallucinogens
psilocybin, LSD, mescaline, MDMA
medical uses of schedule I hallucinogens
depression, PTSD, drug and alcohol dependence, psychological trauma
tolerance of hallucinogens
develops quickly and dissipates quickly
tolerance of MDMA
depression and cognitive deficits
chronic use of PCP and ketamine
memory loss, speech problems, delusional thinking
addictive hallucinogens
PCP, ketamine, MDMA (slight potential)
nonaddictive hallucinogens
psilocybin, LSD, mescaline
opiates
occur naturally in opium poppy
example opiates
opium, morphine, codeine
opioids
natural/synthetic/semi-synthetic/endogenous substances that bind to opioid receptor
recent changes in opioid use
increase due to overprescription and nonmedical usage, as guidelines became stricter, people turned to heroin
most common methods of obtaining painkillers for nonmedical purposes
- given to by friend or relative
and being prescribed by more than one doctor
naturally occurring opioids
coming from opium poppy
morphine, codeine, thebaine
semi-synthetic opioids
chemically modified natural opiates
heroin, Vicodin, oxycontin, Percocet
synthetic opioids
methadone, fentanyl
opioids route of administration
ingested, rectally, sublingually, transdermally, snorted, smoked, injected
mechanism of action opioids
opioid receptors and endogenous opioids
acute effects of opioids
diminish pain, suppress respiration, increase sleep, euphoria, impaired cognitive function
opioid triad
three key signs of opioid overdose
coma, depressed respiration, pinpoint pupils
medical uses of opioids
cough suppressant, alleviate diarrhea
opioid tolerance
metabolic, cellular, behavioral (increased tolerance if its in a location that has repeatedly been used prior), cross-tolerance to other opioids
withdrawal of opioids
symptoms are opposite of direct effects of drugs
pain, irritability, insomnia, diarrhea, dilated pupils
organ impact from opioids
organs are not damaged from long term use but addict lifestyle is most dangerous effect
opioid dependence
addiction due to physical, environmental, and psychosocial factors
substitution opioids
methadone and buprenorphine
harm reduction to allow addicts to function normally and lessen craves and withdrawals
other opioid treatment methods
needle exchange, detoxification under anesthesia
medications to aid opioid dependence
naltrexone, clonidine
most potent opioids
fentanyl, heroin, oxycodone
least potent opioids
morphine (baseline), codeine
sedatives
relieve anxiety, cause relaxation, mild CNS depressants
hypnotics
cause drowsiness and sleep
BZD prevalence
more popular than barbiturates, females to males = 2 to 1 ratio
barbiturates and BZDs more likely to be abused
short acting, lipid soluble
short acting sedatives used for
preanesthetic sedatives or for insomnia
longer acting sedatives used for
anticonvulsants, muscle relaxants, anxiolytics
anxiolytic
kind of medication that eases anxiety
sedative routes of administration
oral, rectal, injection
BZD absorption
less lipid soluble than barbiturates, absorbed more slowly, slower onset of action
BZD trade names
xanax, valium, klonopin, Ativan
metabolism of sedatives
liver with cyp450 system
sedative metabolism decreased in ____
infants, pregnant women, liver disease, elderly
BZD mechanism of action
binds to GABA A receptor in limbic system, reticular activating system, cortex, (not respiration)
barbiturate mechanism of action
more general effect on GABA than BZD
acute effects of sedatives
reduce muscle tone, impair coordination, reduce anxiety, learning, memory, cause bizarre uninhibited behavior
effect of sedatives on sleep
total sleep time is increased by REM sleep and restorative deep sleep are reduced
effects of sedatives on fetus
cleft palate, floppy infant syndrome
sedative drug interactions
other drugs metabolized by cyp450 system
safety of barbiturates
low TI, risk of overdose increased when used with other opioids or depressants
Therapeutic use of barbiturates and BZDs
insomnia, anxiety, seizures, alcohol withdrawal, anesthesia
why have BZDs largely replaced barbiturates?
more specific effects
fewer side effects
wider margin of safety
lower potential for abuse/tolerance
less effect on REM sleep, longer lasting effects have less potential for abuse
z drugs
ambien, Lunesta, sonata
produce sleep rhythm more like natural sleep
increased risk of car accidents, sleep walking/eating/sex/driving
chronic use of sedatives
daytime fatigue, accidents, mortality
sedative tolerance
develops for sedative/hypnotic effects but not for anticonvulsant effects
more common in barbiturates (cellular and metabolic) than BZDs
sedative addiction
barbiturates > BZDs
sedative withdrawal
should be medically supervised
insomnia, confusion, difficulty concentrating
inhalants
substances that have effects similar to sedatives/hypnotics
prevalence of inhalants
younger adolescents
volatile inhalants
glues, aerosols, cleaning agents, fuels
anesthetic inhalants
ether, nitrous oxide
nitrite inhalants
amyl/butyl nitrite
acute effects of inhalants
similar to alcohol intoxication, huffing, sudden sniffing death syndrome, incoordination and recklessness
chronic use of inhalants
nose bleeds, depression, hostility, cancer, damage to organs, cognitive impairments
cannabis prevalence
most commonly used illicit drug in the US (18% in past year)
inverse relationship between use and perceived dangers
cannabis sativa
tall and slender with lighter green leaves
cannabis indica
shorter and bushier and darker leaves
almost all strains of cannabis today are ____
hybrids
female and male cannabis plants
flower clusters with psychoactive resin that catches pollen from male seeds, separating male and female will increase psychoactivity of the plants
phytocannabinoids
THC, CBD
bind to cannabinoid receptors in the body
THC
psychoactive
CBD
anti oxidant/convulsant/inflammatory/anxiety
hemp
trace amounts of THC, not psychoactive
cannabis routes of administration
smoked, vaporizers, ingested (slower onset and less predictability of action)
cannabis absorption
THC is very fat soluble, easily crosses BBB
cannabinoid receptors
CB1 and CB2
THC partial agonist, CBD negative allosteric modulator which blocks some of THC’s effects
cannabinoids bind to other receptors in the body such as _________
GABA, serotonin, glutamate
mechanism of action of cannabis
endocannabinoid system
endocannabinoid system
widespread system that controls physiological effects and helps maintain homeostasis
neurotransmitters of endocannabinoid system
anandamide, 2-AG
function of enzymes of endocannabinoid system
synthesize and break down cannabinoids, endocannabinoids synthesized on demand, not stored
receptors of endocannabinoid system
CB1 and CB2
location of receptors of endocannabinoid system
basal ganglia, cerebellum, hippocampus, amygdala, eye, pancreas, testes, uterus
acute effects of cannabis depend on ____
dose, ration of THC to CBD, previous experience and expectations, environment
biphasic dose response curve
for cannabis, optimal dose receives highest benefits and low/high doses receive low benefits (looks like normal curve)
acute effects of cannabis
euphoria, laughter, impaired memory, impaired coordination, enhanced sensory perception, drawn out sense of time, hunger/thirst, increase heart rate
TI of cannabis
very high, over 1000
negative effects of cannabis
impaired fertilization from high doses, drug interactions, collateral damage from use
medical uses of cannabis
chronic pain, nausea/vomiting, increase hunger, MS symptoms, reduce use of addictive substances, other disorders/conditions
tolerance of cannabis
regular use causes tolerance
addiction of cannabis
less addictive than other drugs, treatment involves psychological approaches, less than 50% stay abstinent
cannabis withdrawal
symptoms are not severe if they occur
primary function of liver in drug use
metabolism
primary function of kidneys in drug use
elimination
reward pathway in the brain
network of structures involved in pleasure, motivation, and reinforcement
two main structures of reward pathway
ventral tegmental area (midbrain, produces dopamine in reaction to rewarding stimuli) and nucleus accumbens (limbic system, receives dopamine and generates feelings of pleasure)
primary neurotransmitter of reward pathway
dopamine
How does methamphetamine differ from other stimulants and other forms of amphetamine?
stronger, longer lasting effect
stronger impact on dopamine release which causes euphoria, much more potential for abuse and addiction