Week 3 Flashcards
The two major aspects of drug influences
Drug effects (observable changes)
sites of action (binding sites)
Pharmacokinetics
What the body does to the drug
Endogenous vs exogenous
Endogenous: made in our body
Exogenous: produced outside our body
Pharmacokinetics vs pharmacodynamics
Pharmacokinetics: how drug moves through body
pharmacodynamics: biological response to drug
Four processes of pharmacokinetics
ADME
Absorption (how get in body)
Distribution (how moves trough body)
Metabolism (how is drug changed to an inactive form my enzymes)
Excretion (drug is excreted in urine by kidneys)
IV: fastest b/c it goes straight into your bloodstream
intraperitoneal: to your stomach (e.g., tubefeeding)
subcutaneous: into your fat
intracerebral: directly into your brain; bypass the blood-brain barrier; not really done in humans but on research animals
intracerebroventricular: straight into CSF
oral: one of the slowest ways; first pass metabolism (broken down in saliva, down to GI tract, etc); most common way for
psychotherapeutic drugs
sublingual: absorbing through capilaries below your tongue
intrarectal: bypassess “first pass” metabolism
inhalation: into your lungs
insufflation: absorbed by the mucous membrane in your nose (e.g.,
snorting cocaine)
Inhalation vs insufflation
inhalation: into your lungs - EX. weed
insufflation: absorbed by the mucous membrane in your nose (e.g.,
snorting cocaine)
- EX. cocaine
Blood flow
Entire volume of blood supply circulates every minute
Where do drugs exert their effects?
Sits of action
Most important factor in determining rate of absorbtion?
Lipid solubility – Lipid soluble materials pass through the most rapidly (pass through BBB)
heroin is more addictive b/c it has higher lipid solubility than morphine
Metabolism of drugs
most drugs are metabolized and deactivated by enzymes.
Enzymes sometimes transform molecules into more active versions
than the initial molecule. THIS INCREASES DURATION
- Ex. Prozac: body changes it to be more active, why takes two weeks to kick in (enzymatic activation)
LIVER: plays big role in enzymatic deactivation
Excretion of drugs
kidney is the primary organ of excretion
(GI, skin, lungs, and liver too)
Effictiveness of a drug is impacted by
sites of action
affinity at its site of action
Affinity: the capacity of a drug molecule to bind to a key site of action.
Affinity ratio for most desirable drug
Most desirable drug has high affinity for sites of action producing
therapeutic effects and low affinity for sites of action producing toxic side
effects
Dose Response Curve
Determines the point of maximum effect of a drug
After point of maximum effect of drug, increasing the dose does not produce a stronger effect
Margin of safety
The difference between therapeutic/desired effect of a drug and undesired effect
want the largest margin of safety
Therapeutic Index
A commonly used margin of safety
Two numbers obtained:
- Effective Dose 50 (ED50) = the dose that produces the desired effects in 50
percent of the individuals
- Toxic Dose 50 (TD50) = the dose that produces toxic effects in 50 percent of the individuals
Want ratio of TD/ED to be bigger than 10
Ex.
Low TI
ex. Lithium, Clozapine, Tricyclic antidepressants
have to get blood tested often
Neurotransmitter vs neuromodulator
Neurotransmitter: a chemical used for a neuron-to-neuron communication
Neuromodulator: a chemical that affects the neurotransmission of a whole group of neurons
GROUP VS INDIVIDUAL
Termination of a neurotransmitters
Through reuptake or enzymatic deactivation/degradation
Ligands
Neuromodulators that bind to a complementary receptor site
Agonists vs antagonists
Agonist a molecule that by binding to the receptor stimulates a
response = ↑ postsynaptic effects
Antagonists a molecule that by binding to a receptor blocks or
inhibits the response = ↓ postsynaptic effects
Is a drug that blocks the re-uptake or enzymatic degradation of a
neurotransmitter an antagonist or agonist?
Agonist! because re-upatake is blocked, the neurotransmitters are jsut hanging in the cleft, still sending signals
If the activation of a receptor causes vasoconstriction, what would happen if someone took an antagonist for that receptor?
Decreases vasoconstriction
