exam 1 Flashcards
what is a drug?
nonfood chemical that alters 1+ biological processes
influence of {drug related things} on drug experiences
- chemical structure: slight diff in chemical compounds cause it to become a diff drug
- drug dosage: the more you take = the more of an impact it has
- time between drug admin: how many hours/days/months pass before taking it again
- frequency: how often within a time period? : related to tolerance
influence of {person related things} on drug experiences
- psychological makeup and expectations: some people should/shouldn’t take drugs, some don’t like it
- experience is often how you expect the drug to be - social and physical environment: drug experiences are diff if you’re alone vs w/ friends or at home vs at a party
- biochemical individual variability: everyone will have diff reaction to same drug bc of differences in biological makeup
jacques joesph moreau
- mid 1800s
- first to investigate drugs and psychological processes (used has to research)
- research in mental illness
ap charvel
- early 1900s
- wrote first book on drugs and animal behavior (drug of choice was opium)
sigmund freud
- used cocaine to treat his own depression
- found that coke is a mood enhancer but doesnt last long
- first to theorize that coke could be used as a topical anesthetic
ivan pavlov
- researched bromides (they relax people but are very toxic)
- experimented on people with schizophrenia, didnt work
william james
- father of psychology
- liked to take nitrus oxide (laughing gas)
albert hoffman
-invented lsd/acid in 1938 (comes from rice fungus)
- attempted to use it to research if it would regulate pregnant women blood pressure
- he spilled it, absorbed into skin, realized it shouldn’t be used for og purpose
good implications of psychopharmacology
- deinstitutionalization of patients ( institutionalized ppl were treated poorly; shock therapy, lobotomy)
- more rigorous diagnoses
- stimulated an interest in relationships btwn the brain, biochemistry, and behavior
bad implications of psychopharmacology
- side effects varied (small or big) and they interfere with drug compliance. more meds given to treat side effects. some tale 3+
- medication reliance: drug usage makes people lazy & will do things theyre not supposed to bc drug will fix the problem anyway
- poor support systems (institutionalized ppl didnt have support once they were let out leading to homelessness or jail)
- diagnosis through medication “take this pill, if it works then you have it” . youre not getting to cause of issue, just bc meds help does not mean you have it
-ethical issues
- perceptions that drugs are not dangerous: just bc doctor gives you a drug does not mean it is safe for overconsumption
does drug restriction / control work? what does it cause?
- trying to outlaw drugs makes problem worse
- violence, overdose, incarceration, addiction all go up while health decreases
harrison narcotics act of 1914
- targeted black and chinese men
- ban on non-medical use and sale of opium and cocaine
what was prohibition? what caused and ended it?
- 1919-1933
- ban on all alcohol (purchasing)
- temperance movement: protestant women wanted alc to be illegal
- ended after stock market crashed, government needed to make money by taxing it
what is the war on drugs?
- begins in the 70s
- president nixon makes all drugs illegal & popularizes the movement
types of drug prevention programs & do they work?
- info based
- social skills “just say no”
- project dare
NO THEY DO NOT WORK
what works to prevent early drug usage?
- putting kids in afterschool activities / occupying their time
- talk to kids in a non judgmental manner / open convo
- community wide, multi dimensional efforts
why are prevention programs popular?
- makes people feel good
- illusion of success: adolescents who go through program dont use drugs, but thats bc most adol. normally dont
concentration of drug at receptor and drug effects
how much of a particular drug is in the area
- drug neurotransmitters need to hook up to a receptor that is then activated or blocked by drug
rate of accumulation at receptor site and drug effects
how much & how quickly are receptors activated
- dosage: quantity
- age: children/old people have less body fat, so they’ll get higher concentration of drug
- species: smaller=higher concentration
- uneven distribution: drugs do not know where to go
pharmacodynamics
biochemical and physiological effects of drugs & their mechanisms of actions
(how drugs effect receptors & how receptors respond)
receptors
proteins that act as binding site for neurotransmitters
- exist in active / inactive configuration
ligands
anything that bonds to something else
ligand affinity
how long / strong can a compound remain bound to receptor
ligand efficacy
degree of biological activity after binding
- how much activity does neurotransmitter / drug cause @ receptor site
ionotropic receptors
- happen quickly / gate opens and closes
- composed of 5 protein subunits: ligands can bind to diff sites on same I. Receptor
- receptor is affected in many ways depending on how many diff types of chemicals are binding to its sites & how can potentially affect how other I.R. are working if they are bound together
Metabotropic Receptors
receptor outside of cell wall –> goes through wall –> hooks up to secondary messenger (G protein)
happens over long periods of time
allosteric modulators
- indirect agonist
- no activity caused @ direct site but can influence other binding sites
ligand - receptor relationship
- every ligand conveys same message to everybody
- some chemicals can not hook up to every receptor
- amount of biological activity can differ depending on the “fit”
key analogy:
- not all keys fit all locks
- some keys fit some locks better
- just bc. key fits. does not mean it will work
agonist
compounds that activate receptor (increase activity)
full agonist
100 % activation
indirect agonist
enhances activity for other ligands
ex: cocaine hooks up to dopamine receptors @ 1 binding site & interferes w/ the re uptake of coke back into cell –> more dopamine in system
partial agonist
between 0 - 100%
- can have higher efficacy for a particular receptor site (can bind stronger than full agonist)
- ex: aripirazole: dopamine agonist, does not reach 100%
inverse agonist
reduces or decreases activity
- ex: valium: decreases anxiety
mixed agonist - antagonist
drug acts as agonist by itself, but blocks activity of other agonist
antagonist
blocks receptor / causes no activity
- high affinity but no efficacy
dose response relationship
relationship between how much of drug is administered and its observed response
placebo influence on dose response relationship & possible ethical issues
control group does not receive the active ingredient
- usually sugar pill
- active placebo: no active ingredient but mimics side effects of drug being tested
ethical issue: no effective treatment is being given / withholding active drug
- “control” can be given alt. med that has been used to treat condition
- not a real CONTROL group anymore
what is therapeutic window?
amount of drug that will cause desired effects but no side effects
what are therapeutic windows reliant on?
response dependence: different drugs have different therapeutic windows
drug dependence: every drug has diff level of toxicity and plasma half lives
no typical dose response function: every person has diff dose response relationship to a drug
plasma half lives
how long it takes to eliminate half of drug from blood stream
threshold dose
smallest dose that produces detectable change
maximum response
greatest degree of a response that can be achieved w/ drug or its full potential
median effective dose (ED50)
dose that produces desired effect in 50% of people tested
median lethal dose (LD50)
dose that kills 50% of subjects tested
therapeutic index
divide lethal by effective
- if index is <100 then it is safe
median toxic dosage
dosage that 50% of people start to experience side effects
maximal therapeutic response
when a drug is most effective at a dose with minimal side effects
dose response efficacy
how effective is drug @ producing a given effect relative to maximum response
clinical efficacy
how long does it last?
is it worth it?
side effects?
magnitude of desired effects?
potency
ability to produce particular effect due to dose size
potency: side effects
how much do we give and what are the side affects associated
potency: administration
more potency affects how we take it
more potent the drug = smaller the pills / lower dose
antagonism
2 drugs in system
- 1 drug reduces potency of other
competitive antagonism
1 drug w low efficacy binds to receptor and doesnt allow another one to hook up to same receptor
noncompetitive antagonism
binds so tight to receptor it cant be unbound
physiological antagonism
2 drugs that act at 2 different receptors but have diff biological actions
ex: vodka redbull
- redbull increases heartbeat
- vodka decreases heartbeat
synergism
potency increases when 2 drugs are combined
synergism: addition
2 drugs taken together, overall response is exactly like having the 2 together
2+2=4
synergism: potentiation
2 drugs, they are greater than what is achieved by each independently
2+2=5
pharmacokinetics
what does body do to drug?
- metabolism & elimination
blood brain barrier
semi-permeable membrane: separates blood in brain from the other fluids of the brain tissue
- its capillaries (astrocytes add layer to capillary) are diff compared to rest of body
- only allows somethings: have to be lipid soluble
lipid solubility
- fat soluble
- high l.s = faster absorption into brain to blood brain barrier
oil/water partition coefficient
ratio of lipid to water solubility
- equally soluble in water and fat
- lipid soluble gets into brain
- water soluble gets into blood
- high oil and low water needs an aqueous vehicle too travel into blood stream
ex: alcohol has a 1:1 ratio
- about 15 sec for alc to effect the body
per os (P.O)
means by mouth
- gut —-> liver —> blood —-> brain
- most common, safest, most convenient
- slow absorption
- patients must be conscious
- slow rate of absorption can limit drug effectiveness
- variability of absorption is based on body fat
- can irritate the stomach
inhalation
- lungs —> blood —> brain
- meds, smoking cigs or weed
sublingual / buccal administration
- under tongue / absorption through oral membrane
- ex: through the gums (zyns) , chewing gum, drops on tongue
transdermal transport
- through skin
- patch
- rare: not many drugs can be absorbed into skin
intravenous
- into vein
- fast
- can OD easily
- requires aqueous vehicle
- vessel irritation: bruises, irritates blood vessels, veins can collapse bc they cant hold shape
intramuscular
longer needles needed to get to muscle
- ex: botox, epi pen, rabies vacc
subcutaneous injection
underneath skin, below top layer
- allergy shots, insulin
intradermal injection
JUST BARELY underneath skin
- allergy testing
intraarterial
arteries
- typically the biggest (femoral)
- ex: cancer drugs
bone marrow used as route of admin bc
babies: veins are too small
or if person has collapsed veins
intranasal used as route of admin for
nasal meds
cocaine
some cold meds
rubbing into skin used as route of admin for
- rare
- topical steroids
intrathecal used as route of admin when
between vertebrae into spine
- ex: epidural
intracerebroventricular used as route of admin to..
- ventricles in brain
- used to get cerebral spinal fluid
-not common, more for research
intraperitoneal
- the gut area; needle through abdomen
- rare
- ex: ozempic
- more used in vet medicine than humans
drug distribution in tissue
through adipose tissue (body fat)
- sex differences: women have more body fat than men
- more body fat= lower water in blood
drug distribution and plasma proteins
drugs combine to blood proteins and can displace other drugs
catabolism
breaking something down into smaller parts
anabolism
to make bigger / more complicated
ex: anabolic steroids (make muscles bigger)
first pass metabolism
through the liver (hepatic microsomal enzyme system)
- P450 enzymes : cleanse our body of toxins ( not selective )
first order kinetics
more drug in system = more metabolism
zero order kinetics
drug amount does not matter, will be metabolized at constant rate
- ex: alcohol
influences of drug metabolism
other drugs
-enzyme production: it is affected by taking 2+ drugs
- ex: barbituates and alcohol: enzymes will attack barb and ignore alc, so it will hit harder
- shared metabolic pathways: some drugs can alter metabolized form of other drugs
age
- children and old people have fewer p450 enzymes & body fat
nutrition, disease, and sex
methods of drug excretion
urine, feces, glands, breast milk
pregnant women:
- pass through placenta and into baby’s developing brain
- baby’s get higher proportion of drug in blood system compared to mom (ex: alcohol)
- babies are predisposed to physiological and psychological deficits bc of drugs mom takes (includes prescription)
central nervous system
control unit
- brain, brain stem, and spinal cord
peripheral nervous system
body link to outside
somatic nervous system and two types of nerves
interaction btwn external stimulus and brain
- afferent: sensory info to the brain
- efferent: motor info to skeletal muscles
autonomic nervous system 2 parts and 2 types of nerves
controls involuntary functions
- afferent nerves: internal organs to brain
- efferent nerves: brain to internal organs
- sympathetic ns: fight or flight (can also inhibit)
- parasympathetic: rest & digestion (can also stimulate)
conduction
transmitting info within the cell
transmission
neurons talking to each other
parts of a neuron and their functions
- dendrites: receive signals from neurons
- nucleus: holds DNA
- myelin sheath: fatty layer, increases speed of sent message
- axon: conducting fiber / transmits electrical impulses away
- axon terminals: transmit signals to other cells
- synapse: gap btwn axon terminals and dendrites
schwann and oligodendrocyte
what they do
where they are found
both create myelin
- schwann cells found in pns
- oligodendrocyte found in cns and prevents nerve regeneration
somatic nervous system
- found in pns
- interaction btwn external stimulus and brain
- afferent: sensory info to brain
- efferent: motor info to skeletal muscles
automatic nervous system
- found in pns
- controls involuntary functions
- afferent: internal organs to brain
- efferent: brain to internal organs
sympathetic and parasympathetic
sympathetic: fight or flight
parasympathetic: rest and digestion
both found in automatic nervous system
glial cells
nourish and protect neurons
astrocytes
type of glial cell
- helps create bbb
resting potential
membrane of neuron isnt transmitting signals
- negative inside
- polarization is negative 70mV
sodium potassium pump
- inside of cell has potassium (+) and chlorine (-)
- outside of cell has sodium (+)
- the pump tries to maintain testing stage
- allows potassium inside cells and keep sodium out
concentration gradient
difference in ion concentration
- flowing from high to low concentration
electrostatic pressure
force that pushes ions into oppositely charged area
- positive ions are attracted to negative ions inside cell
- why sodium wants to go inside cell
excitatory vs inhibitory postsynaptic potentials
excitatory: tell them to create an action potential
inhibitory: no action potential
spatial vs temporal summation
spatial: how many different postsynaptic potentials are touching at any given time
temporal: how quickly are signals being received
- slow = weak
axon hillock
decides if action potential happens
- found where axon and cell body meet
- if excitatory outweighs inhibitory then action potential occurs
voltage activated channels
- action potential: gates open and allow sodium inside and polarization is +50 ; it is depolarized
- gates then close and start s.p pumps starts kicking out sodium and bring polarization to -90
- neuron is hyper- polarized, making it harder to create another action potential
absolute refractory period
neuron cant fire /create another action potential
- lasts milliseconds
- keeps signal from reversing
- signals (action potential) jumps from node (of ranvier) to node
relative refractory period
neuron is hyper polarized
- more stimulus is needed
- conserves energy
synaptic transmission
- direct synapse
- activates and deactivates quickly
- sensory motor : faster
types of synaptic transmission
axondendritic synapse: where they release / connect to receptor is very small
axoaxonic: synapse between 2 axon terminals
axosomatic: synapse between axon and cell body
non synaptic neurotransmission
non direct synapse
- distance between release & receptor site is far
- mood states & arousal
- last longer
- attach more strongly than directed synapse
- peptides generally
retrograde neurotransmission
1 neuron releases neurotransmitters to another, and 2nd neuron releases neurotransmitters back to 1st neuron
- feedback loop: increases relationship btwn 2 neurons
- if neuron doesnt fire back, a new pathway is created to find new neuron
small neurotransmitters
activate on direct synapse
- release quickly
- cause brief responses
- act but also stop working quickly
large neurotransmitters
- peptides (made of 2-10 amino acids: building blocks of protein)
- released more gradually
- effects last longer
coexistence
1 neuron contains both small and large neurotransmitters
co transmitters
different neurotransmitters are stored in diff types of vesicles and get released depending on how sodium is in cell
- not all are released at once, depends on polarization
exocytosis
release of neurotransmitters
termination of neurotransmitter effects
- diffusion: floats away
- re uptake: sucking up released n.t back into neuron (the ones that dont float away or dont connect to a receptor)
- enzyme degradation: breakdown n.t @ receptor sites
glial cells: kick it off receptor
autoreceptors
receptors on presynaptic neuron that hooks up to own n.t
- inhibitory feedback: tells neuron if it released too much n.t and will adjust for next time
- on cell and dendrites: hyper polarizes cell
- on axon terminals: modifies production of n.t and how much is released next time
nonsynaptic neurotransmission diffusion
diffuses through extracellular fluid and cerebral spinal fluid (ecf & csf)
its receptor affinity is stronger that a direct synapse
