Introduction to Drugs and Behavior Flashcards
drug use
many animals (humans and others) ingest substances that change the way the mind and body work
psychopharmacology
the study of how drugs affect mood, perception, thinking or behavior
psychoactive drugs
drugs that affect mood perception, thinking, and/or behavior by acting on the nervous system ex. cocaine
Who cares?
many people in this room
recreational drug use (misuse)
drug use to treat psychological disorders/difficulties
recreational drug use (misuse)
impacts on behavior and function
in many cases, person is by definition a criminal
drug use to treat psychological disorders/difficulties
How do psychological drugs work?
How do they change/alter the subjective experience of the person using?
statistics
lots of people use drugs
Who is a psychopharmacologist? (PsychoPharm)
medical practitioners
researchers
behavioral pharmacology
medical practitioners
psychiatrists- prescribe drugs as part of treatment of psychological disorders
researchers
study the effects of psychoactive drugs
behavioral pharmacology
Subfield of Applied Behavioral Analysis
Drugs= stimulus from the environment
What is a drug?
A substance, other than food, that when ingested/administered, alters the way the mind/body works
administered drug
not produced naturally by the body
dopamine
neurotransmitter produced by the body- not a drug
substance given by a psychiatrist to treat auditory hallucinations- is a drug
psychoactive drugs instrumental use
using a drug for a specific purpose
usually occurs with psychotropic drugs
drugs used for treating mental disorders
can also be non-medical
drinking coffee to “wake-up”
psychoactive drugs recreational use
using a drug to experience its effects (for “fun”)
drinking alcohol to get a “buzz”
drug misuse- drugs that are meant to be used instrumentally- that are used recreationally.
What’s in a name?
Nearly all therapeutic drugs have a generic name and (at least one) brand name
brand name: trademarked name
generic name: non-propriatary name that indicates
- classification for a drug
- distinguishes it from other drugs in a class
ex. tylenol (brand name) vs. acetaminophen (generic name)
generic names
tell you about the class of a drug
ex. chlorpromazine vs. clozapine vs. olanzapine
all 3 drugs end in “a” followed by a consonant and the suffix “ine”
drugs with “apine” or “azine” in their names= antipsychotics
this also tells us something about the chemical structure of the drug
INE suffix= amine chemical in their structure
this isn’t always true- but ideally the generic name tells us a bit about the drug
chemical name
details the drug’s chemical structure
“street names”
usually for recreational drugs..
benign sounding words-
keeps others from understanding what is going on
ex. MDMA= Adam
sometimes the effect of the drugs
ex. MDMA= ecstasy
doses
dose= amount of drug/body weight
in experimental settings- we may give an animal 1.0 g/kg
- avg lab rat weights 500 gs
- dose= 0.5 g
for OTC drugs (over the counter)
- drugs assume an avg adult’s body weight
- take 1-2 tabs every 4-6 hours
- this has created a lot of controversy in medical research
dose-effect curves
shows the effects of drug affected by dose
different drugs produce different responses
lower doses
weaker responses
higher doses
stronger responses
what is EC50?
the value at which “50 percent” of an effect was observed
can be other values
measure of potency of the drug
potency
amount of drug used to produce a certain level of effect
the drug is considered “higher potency” when it takes a smaller amount to reach EC50
toxic dose
the dose that causes unacceptable adverse effects
TD
the point at which 50% of subjects experienced toxic effects of a drug
therapeutic index
ratio of drug’s toxic dose-effect curve relative to the therapeutic dose-effect curve value
any drug is going to have adverse effects
how do we determine if the therapeutic effects of a drug outweigh the toxic effects?
therapeutic index graph
distance between toxic and therapeutic doses
ratio of TD:ED
divide TD by ED
how different is a dose that causes toxic effects in 1/2 Ss from a dose that produces therapeutic effects in 1/2 Ss
Ss
subject or participant
certain safety index
calculated by dividing a TD1 (1 percent) by the dose that achieved ED99
this is a more conservative estimate
the FDA requires safe therapeutic indexes for approved drugs
not every drug has a large therapeutic index
lithium (bipolar disorder)
the lethal dose is very close to the therapeutic dose
often people using these drugs are closely monitored for toxic effects
when 2+2=5
when you take more than one drug- they may influence each other
additive effects
the magnitude of the combined drug effect (Drug A+ Drug B) is the sum of each drug’s effect alone
Drug A increases systolic blood pressure (BP) 5% and Drug B increases BP by 10%
A+B increases BP by 15%
synergistic drug effects
the magnitude of the combined drug effect is greater than Drug A+B
E.g. Advil (ibuprofen) + Tylenol (acetaminophen) = more pain relief
2+2=5
pharmacodynamics
the physiological & biochemical reactions of drugs
cannabis makes you feel euphoric and makes eyes red
mind and body
pharmacokinetics
how drugs pass through the body
administration (how do you take it?)
duration of effect
how does it enter the brain?
why is heroin more addictive than morphine?
gets through the blood brain barrier- the semi-permeable barrier at the molecular level- brain does not know that heroin is potentially dangerous
pharmacogenetics
the study of how genetic differences influence a drug’s influence a drug’s pharmacokinetic and pharmacodynamic effects
helps to provide the basis of differences in drug responsiveness may affect how that drug affects the nervous system, is processed by the body
pharmacogenetics and pharmacodynamics
some genes make people more susceptible to using a drug
pharmacogenetics and pharmacodynamics example
30% of population has cannabis use disorder
Gene on chromosome 8 (controls levels of gene CHRNA2)
Low levels of this gene expression in the cerebellum = associated with cannabis use disorder & diagnosis at an earlier age. (NIDA. (2019, January 14))
BUT- genes don’t “make” you addicted.
pharmacogenetics and pharmacokinetics
fast metabolizer vs. slow metabolizer
based on genetic make-up (not tolerance/learning)
fast metabolizer
people whose bodies break down drugs faster than “normal”
results: less drug in the system and weaker drug effects
can be measured through blood samples
slow metabolizer
bodies break down compounds much more slowly
can lead to toxic effects
objective effects
The effects that can be observed by others (and replicated)
E.g. heart rate increase when you take cocaine
subjective effects
how a person feels while using a specific drug
often more useful than objective effects
measured by individual surveys based personal feelings
need to know subjective experience if:
use the drug for therapy
does it make an anxious person less anxious?
might be used recreationally
does this drug feel good?
measures of the body would be objective, therapeutic effects would be subjective
observational studies
measures behavior as it naturally occurs
correlational studies
do changes to one variable predict changes to another variable
collect 2 data points for each Ss
do some math and get a number
number will tell you 2 things
strength of the relationship (1.0-strong->0.01 weak)
direction of the relationship (+/-)
Ex. relationship between # of times you have a Ss used MDMA and the number of items remembered from a word list
-1.0 strong negative relationship
0 weak
+1.0 strong positive relationship
experimental studies
independent variable (IV)- at least 2 versions (factors)
experimental manipulation & control
dependent variable (DV)- what you are measuring or counting
How do changes to the IV lead to changes in DV
How do to you manage people’s expectations?
when people are given a pill, they know they receive a pill
sometimes- thinking something is real can lead to you behaving like it’s real
- think about a bump in the night, fake needles
you want your control group & experimental group to be as similar as possible, SO
equate expectations between groups
placebo= fake treatment
If you are treating Disorder X with a new drug… Group A gets the drug, Group B gets placebo
If Group A gets better and B does not - results are likely due to the drug.
single blind procedure
Ss don’t know which condition they are in (treatment or placebo)
Prevents biased responses
Told about possible consequences of using the experimental drug and that they may receive a placebo
double blind procedure
neither they Ss OR the experimenter (explicitly) know which condition participants are in
ensures all groups are treated equally
open label
not a blind procedure
it can be unethical to withhold a specific drug/treatment and give placebo instead
E.g. cancer, severe mental illness, etc.
internal validity
adequacy of controlling variables that may influence a dependent variable
participants unknowing what the study is about- if they learned it was a placebo it would be a threat
external validity
ability to extend findings beyond study conditions
represent large populations- only studying a small group that should be applied to the whole population
face validity
test appears to measure what a researcher considers it to measure
measuring heart rate to predict cardiovascular health
construct validity
how well a study’s findings relate to the underlying theory of a study’s objectives
results matching theory
hippocampus involved in memory study- getting rid of hippocampus to see an affect on memory
theory must be involved
relating question of variables to what you’re actually testing
serotonin based on instagram usage- wouldn’t use snapchat- variables involved
predictive validity
ability of model to predict treatment effects
ability to predict how you will react to a drug/situation in study
if you know a subject well can you predict how they will react
stage 1: what to treat?
this is an economic decision
How much research is available?
How many people are affected by this disease/problem?
Will this treatment “pay-off”/make a profit
stage 2
chemists develop experimental compounds
stage 3
test compounds developed in stage 2 with biological models
e.g. how well does this bond to tissue?
prefer to use “high throughput screening methods”
high throughput screening methods**
rapid testing using a large number of experimental drugs
provide quick results and determine if experimental drug=desired effects
chemists then refine and test again- hopefully getting closer to desired effects
stage 4
shift to highly focused screening methods
much slower- but offer greater precision about effects
use models that have face, construct, or predictive validity- often include animal models
stage 5 - safety pharmacology
identify drugs’ toxic effects- can include physiological and psychological
is TD significantly higher than Therapeutic dose?
phase 1 of clinical trials
looking for adverse effects
low dose to healthy population
phase 2 of clinical trials
find preferred population (higher dose and short period)
early short term effects of drug
phase 3 of clinical trials
longer term trials (varying dose, given long term)
phase 4 of clinical trials
FDA approved drug now on market (dose based on phase 3)
participants with disorder to be treated
