Midterm Flashcards
Etiologies of Addiction
Personal responsibility/moral– person is of blame,root of stigma
Agent–blame substance
Genetic/biological
Social learning
Sociocultural
Disease**
What is addiction?
a chronic disease of brain reward, reflected in pathologically seeking out substance
* Organ= brain, defect in reward system (midbrain, prefrontal cortex–>fight vs. flight system, logic system)–> bx: inability to stop using substances, despite harmful consequences–> impact: continued SU, cravings (response when drug cut off), impulsive decisions
Frequency, compulsion, persistence despite adverse consequences
neuron
signal processor
synaptic cleft
space b/w neurons
axon
sender
dendrite
receiver
reuptake
recycle/reuse
neurotransmitter
signal
dopamine
pleasure/feel good
prefrontal cortex
logic/thinking
midbrain
fight vs flight
neuroflooding
“being high”–lots of neurotransmitters in the synaptic cleft
dependence
brain is functioning only when the substance is present; you become dependent on the presence of a drug–body adapts, requiring more to maintain a certain effect (tolerance), eliciting drug/mental symptoms if use stops
tolerance
requiring more for same effect
why? our bodies seek BALANCE, to level off neurotransmitter levels, we kill off endogenous neurotransmitters, receptor down regulation, or deactivate receptors b/c we come to expect external source of substance in high doses
withdrawals
lack of needed neurotransmitters
why? body became dependent on substance, when you no longer provide body w/ external source, your body adapted by down regulating receptors or killing endogenous ones, balance is OFF–> withdrawal symptoms (explains anhedonia)
anhedonia
inability to feel pleasure
Why? you have fewer receptors than you originally did, you may have lower endogenous levels of dopamine being released–>not producing same effects as your brain pre-substance use
hypofrontality
inability to use prefrontal cortex
stress–> activation of fight vs. flight–> deactivation of prefrontal cortex–> seeking out dopamine to help deal with stress–> cravings–> SU
cravings
natural response d/t cutting off a substance
9 areas of treatment planning (HELMMSSDF)
housing, ed/vocational, legal, medical, mental health, social/leisure, SU, D/C, family
problem statement
should reflect 9 problem domains; written in bx terms
goal
pt’s words, strengths-based, presence vs. absence, compliments problem definition
objective
what will the pt do to accomplish their goal, SMART, action terms
Intervention
compliment objective, therapists portion, must include frequency
ASAM
numbers represent benchmarks a continuum, meaning pts move up or down in terms of intensity
6 dimensions of ASAM
-acute intoxication/withdrawal/SU hx
-health (physical)
-psych/mental health
-readiness to change
-relapse, continued use
-recovery/living situation
Order of treatment
referral–> screening–> assessment–> diagnosis–> decide
screening
detect possible presence of problem and need for further evaluation
OARS= motivational interviewing
O: open ended questions
A: affirm
R: reflective listening
S: summarize
RULE= motivational interviewing principles
R: resist telling clients what to do
U: understand motivations
L: listen with empathy
E: empower
SMART= treatment plan goal setting
S= specific
M= measurable
A= attainable
R= realistic
T= time-frame
FRAMES= SF
F= feedback
R= responsibility for change
A= advice
M= menu of options
E= empathic counseling style
S= self-efficacy
ATL
Ask, Tell, Listen
precontemplation
(pros> cons): no intention to change bx, not even on mind
contemplation
(pros= cons): I’m thinking about change
preparation
(pros of use< cons): I am intending to change
action
(pros of abstinence> cons): I am successfully changing bx
maintenance
(pros of abstinence> cons): I am remaining free from bx, >6 mos
termination
end of cycle, no temptations, 100% confident in all previous situations; years of maintenance
Narcan mechanism of action
reverses overdose by…
OPIOID RECEPTOR ANTAGONIST–>binds to opioid receptor and reverses/blocks effects of other opioids (higher affinity compared to opioids)
Suboxone mechanism of action
- Buprenorphine= partial agonist–>producing fraction of rxn as other opioids, weaker rxn–>no high, but no withdrawals, block other opioids from attaching
- Naloxone= antagonist–>block reaction–>used in suboxone to deter intravenous use–>if person tries to inject suboxone intravenously, naloxone will block opioid receptors–> immediate withdrawal symptoms w/o high
semi-synthetic opiod
modification of an opiate (natural); ex: morphine heroin
synthetic opioid
chemically derived in lab; not derived from poppy
opioid
(all-encompassing natural+ synthetic+ semi-synthetic)
opiate
(derived from poppy)
opioid mechanism of action
o Opioid receptor agonists
o Bind to opioid receptors–impact on Ca channels– release of dopamine– euphoria+ other effects
o Half life= .6-150 hours
opiate exames
opium, codeine, morphine
semi-synthetic opioid examples
heroin
hydrocodone
oxycodone
oxymorphone
buprenorphrine
synthetic opioid examples
methadone
fentanyl
tramadol
meds can address (opioid)
withdrawals, cravings, aversion therapy (intravenous), psych disorders, “maintenance”, overdoses (narcan)
DSM mild, moderate, severe
2-3= mild
4-5= moderate
6+= severe
screening tool examples
CAGE, CRAFFT, S2BI, TAPS, UA
