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What characteristics differentiate addiction from regular use of a drug?
chronic use compulsive drug-seeking use despite harmful consequences
Is addiction a medical diagnosis? If not, what is the term used to medically diagnose drug problems?
it is NOT a medical diagnosiscalled "substance use disorder" in the DSM 5
What does it mean when someone says that addiction is a brain disease?
because changes in brain structure + function are fundamental to the development and expression of addiction
prevalence
the proportion of persons who have a condition at / during a particular time period
incidence
the proportion / rate of persons who develop a condition during a particular time
morbidity
the condition of having a disease, illness, or other health problemthe presence + burden of sickness / injury in a population
mortality
the state of being subject to death the occurrence of death w/in a population
epidemic
the rapid spread of disease to a large number of hosts in a given population w/in a short period of time
YPL (???)
years of potential life
DALYs
Disability-adjusted life year:
A measure of the total burden of disease in a population
Quantifies the number of years of healthy years lost to illness, disability, or premature death
attributable fraction
the proportion of incidents in the population that are attributable to the risk factor
what is the approximate prevalence of Alcohol Use Disorder in US in 2015?
6.20%
what is the approximate lifetime prevalence of Alcohol Use Disorder in the US?
10%
Which drug has highest total costs associated with its use?
tobacco + alcohol
How do harms and costs associated with legal drugs compare with illegal drugs?
illegal drugs are cheaper but more harmful
What are areas of cost (for example, healthcare costs, lost productivity, legal costs) are associated with illegal drug use?
direct + indirect costs attributable to illicit drug use are estimated in 3 principal areas:crime, health, productivity, healthcare costs, legal costs
Approximately what percentage of deaths worldwide attributable to alcohol?"
6%
percent of accidents and disability worldwide due to alcohol
around 5%
What is person-first language? Why is it important to use respectful terms to describe people with drug and alcohol problems?
a communication style that emphasizes a person's identity before their health condition, disability, or other defining characteristicsto focus on an individual's humanity rather than defining them by a diagnosis like SUD
What are traditionally accepted uses for psychoactive substances?
spriritual, medicinal, therapeutic uses
When and why did availability and potency of drugs change from the 14th to 20th centuries?
in history, availability + potency was limited to geography, scientific knowledge, tech, and sometimes povertyrecreation use of drugs (other than alc, tobacco, marijuana, and caffeine) were mostly unknown til the 19th century + expanded in the 20th
two main models of addiction that have dominated for thousands of years?
moral model disease model
moral model of addiction
humans are given free will forces of temptation/evil exist to text humans
a virtuous person abstains from / exerts control over temptation/evil
a person that does not is seen as weak, spiritual disfavor, evil, etc.
it is a defect of a person's character for which they are responsible
disease model
views addiction as a primary, chronic brain disorder involving dysfunctional brain circuits,leading to compulsive drug use despite negative consequences
What was the temperance movement in America?
Organized effort to limit or outlaw the consumption and production of alcoholic beverages in the United States
What change to the constitution did the temperance movement produce?
18th amendmentestablished the Prohibition Era by banning the manufacture, sale, and transportation of alcoholic beverages
When was Alcoholics Anonymous founded and by whom?
Bill Wilson and Dr. Bob Smith founded Alcoholics Anonymous in Akron, Ohio in 1935
What influence did the AA model have on the development of the early modern disease model?
popularized the idea that alcoholism is an "illness" rather than a moral failure Jellenick's model
What are the 4 stages of Jellenick's model?
Pre-Alcoholic
Early Alcoholic
Middle Alcoholic
Late Alcoholic
Jellenick's model: pre-alcoholic
social drinkingas stage progresses
drinking is more frequent for stress reduction
physiological char.: beginnings of tolerance
Jellenick's model: early alcoholic
growing discomfort w drinking comboed w an inability to resist it
lying abt drinking to friends/loved ones
spiking coffee, hiding drinks
increased tolerance
increased obsession w thoughts of alcohol first alcohol-related blackout occurs in this stage
Jellenick's model: middle alcoholic
symptoms become obvious to others
missing work/social obligations bc of drinking/hangovers
drinking at inappropriate times (driving, at work, while caring for children)increased irritability + argumentativeness
facial flush, weight loss/gain, bloating attempts to stop drinking
Jellenick's model: late alcoholic
serious health problems develop
everything in life (friends, family, work) take a backseat to drinking
attempts to stop drinking may be characterized by tremors / hallucinations
can be helped w therapy, detoxification, and rehabilitation
First psychological models of addiction
freud: drug use as a coping strategy + form of regression
behavioral: reinforcement → positive reinforcement at first and then negative reinforcement later along w classically conditioned context effects
Modern disease model
the idea of addiction as a disease
IN CONJUNCTION WITH: neuron communication mechanisms + how drugs alter this + behavioral effects caused by the changesreward pathways + how they are affected by the pleasurable sensationst hat drugs produce
Volkow and Li's (2004) v. Armstrong's (2019) models of addiction
Volkow and Li (2004)
focus on neurobiological cycle of drug use frames it as a chronic, relapsing brain disease
Armstrong (2019)
adds an evolutionary + behavioral context to explain why these neurobiological processes are vulnerable to addiction
evolutionary: "ancient reward systems" that drugs are satisfied by + ill-equipped to resistsocial attachmentgenetic predisposition
both
recognize addiction as a brain disease involving the cycles of binge / intoxication, withdrawal, and craving
Why was DSM system created in the first place?
designed to get practitioners to use a common set of criteria
How was addiction thought of in the first version of the DSM?
Symptom of an underlying personality disorder
How was addiction thought of in the second version of the DSM?
More biologically driven
Symptoms still not clearly delineated
risk factor
a factor that is associated with increased likelihood of developing a SUD
protective factor
a factor that lowers a person's risk of developing a SUB
bronfenbrenner's ecological systems model
microsystem: social systems closest to individs
mesosystem: number and strength of interactions BETWEEN microsystems
exosystem: social systems in which the individual is affected by
macrosystem: societal blueprints for culture / subculture
How is understanding bronfenbrenner's ecological model important in understanding risk for substances use?
explains how drug addiction is developed + maintained by the interplay of an individual's environments /systems
central nervous system
brain + spinal cord
peripheral nervous system
the sensory + motor neurons that connect the CNS to the rest of the body (nerves)
name all parts of neuron involved in neurotransmitter communication
cell nucleus
dendrite
soma
axon
myelin
axon terminal
synapse
what part of the neuron is also called the cell transmitter?
axon
what part of the neuron is also called the cell receivers?
dendrites
resting potential
70 millivolts
inside of cell is negative relative to outside of - neuron
threshold of excitation
55 millivolts triggering of action potential
what is the primary anion in neural impulses?
Cl
what are the primary cations in neural impulses?
Na + K
what leads to the release of a NT?
action potential travels down neuron + arrives at the axon terminal
action potential triggers the opening of voltage-gated Ca2+ channels is triggered
Ca2+ flows into the cell in response
Ca2+ synaptic vesicles fuse w pre-synaptic membrane
NT is released
ion channels open when NT bondion flows cause change in postsynaptic cell potential ion channels will close as NT is broken down / taken back up by presynaptic cell
inhibitory NT
discouraging the cell from firing
excitatory NT
encourage cells to fire
major NTs associated with psychological effects
serotonin
norepinephrine
dopamine
glutamate
GABA
acetylcholine
which NTs are found scattered through the brain?
glutamate + GABA
which NTs are found in neural circuits?
GABA
CCK
epinephrine
what is the primary excitatory neurotransmitter system?
glutamatergic system: uses glutamate as a primary excitatory NT
glutamate is most abundant + widely distributed in the CNS
What does the reward circuit do?
collection of brain structures and neural pathways that are responsible for reward-related cognition
primary NT in the reward system
dopamine
where does the reward circuit start and where does it go?
ventral tegmental area (VTA)
through nucleus accumbens
projecting into frontal
pharmocodynamics
the study of how drugs affect the body
pharmacokinetics
the study of the way the body processes + breaks doewn drugs
why is an understanding of both pharmacodynamics and pharmacokinetics important in addiction studies
so that we can understand the effects of a drug
3 R of drug action
release
receptor binding
removal / reuptake
3 R of drug action: release
drugs can increase / decrease NTs release
3 R of drug action: receptor binding
competitive binding: drugs can bind to the NT receptor and mimic / block NT effects
non-competitive binding: drugs can bind to an alternate site on the receptor + modify NT effects
3 R of drug action: removal / reuptake
drugs can promote / inhibit the removal of NTs
affinity
a measure of a drug's ability to bind to a given receptor typealso thought of as "stickiness" or preference
efficacy
a measure of a drug's ability to activate a receptor once it binds
ligand
a mlcl that binds to a receptor
selectivity
"the "pickiness"" of a neuron
only responds to ligands in particular orientations
agonist
a substance which initiates a physiological response when combined w a receptor
agonist examples
opioids:
heroin
fentanyl
morphine
antagonist
a substance that interferes / inhibits the physiological action of another
antagonist examples
naloxone
naltrexone
atenolol
tolerance
the body getting used to a drug causing a reduction in its effectiveness
why does the body develop a tolerance to a drug?
bc the number of sites/cell receptors that the drug attaches to/affinity between the receptor and drugs decreases
what is the benefit of tolerance?
fewer side effects as your body gets used to the medication
3 mechanism by which tolerance can be developed
down regulation
receptor-effector uncoupling
activation of opponent processes
parts of pharmakokinetics
absorption
distribution
metabolism
excretion
how is the duration of drug effects determined
how fast drug is broken down / removed from synapse
how quickly it is metabolized + eliminated from bloodstream
why are drugs addictive?
bc they ware rewarding
what parts of the brain are stimulated to give drugs a "special place" in memory and behavior in addiction?
reward system affects
limbic system
sensory and motor cortex
cerebellum
Why does withdrawal occur with some drugs on cessation of long-term use?
Withdrawal worsens addiction because users want to resume taking the drug to the end withdrawal symptoms
What is withdrawal?
the discomfort and distress that follow discontinuing the use of an addictive drug
How are withdrawal effects specifically related to the effects of the drug itself?
sharply reduces the number of dopamine receptors in brain's reward system
What is the most dangerous withdrawal?
alcohol sweating, rapid pulse, tremors of hand, fleeting hallucinations/illusions, insomnia, nausea, vomiting, agitated behavior, anxiety, and possible seizures
When are the Central Nervous System depressants considered sedatives vs hypnotics?
sedatives: drugs that decrease activity + have a calming/relaxing effect
hypnotics: drugs used mainly to cause sleep
DOSE:
lower dose = calming
higher dose = sleep
psychoactive substance
chemicals that alter a person's mood, level of perception, or brain functioning
alcohol: class of drug
CNS depressant
alcohol: primary NT affected
increase GABA (inhibitor)
serotonin (mood + sleep)
glutamate (memory + blackouts)
alcohol: which R?
release
increase GABA (inhibitor) activity
alcohol: agonist / antagonist ?
agonist
alcohol: cross-tolerant drugs?
possibly but probably not
alcohol: primary effects
at lower BAC lvls: complex + abstract behaviors are disrupted
at higher BAC levels: simpler behaviors may be affects
alcohol: prod a significant tolerance?
yes
alcohol: withdrawal? symptoms?
6-17 Hours: Mild Symptoms
Anxiety, irritability, and craving
17-48 Hours: Moderate Symptoms
Increasing emotional volatility, fatigue, and shakiness
48-72 Hours: Severe Symptoms
Severe tremors, delirium tremens, and seizures
benzodiazepines: drug class
CNS depressant