Unit 1- Intro, Routes Of Admin and Receptor Theory Flashcards
two types of drug names
trade vs generic
generic name
nonproprietary- chemical name of a compound approved by the FDA i.e. ibuprofen
-PANCE
trade name
proprietary name (trademark)
pharmacology define
study of drugs in the body, including interactions between drugs
-dynamics + kinetics
pharmacodynamics
mechanism of action (MAO) of the DRUG in the body
“what does the drug physically do to the body”
i.e. ethanol- loss of inhibition, slurring of speech
pharmacokinetics
what the BODY does TO drug
-absorbs, distributes, metabolizes or excretes
T/F effects of drug vary by pt
true
the relationship between drug conc. and effect on body
pharmacodynamics
effects of a drug can either be ____ or toxic
therapeutic/efficacy
pharmacogenomics
define drug
any substance that brings about a change in biologic fx through its chemical ax (key)
receptor
component of a cell or organism that interacts with a drug
what is known as a lock and key
receptor vs effect of drug
where can a receptor be located?
intracellularly or on the surface
what initiates the chain of biochemical events and what does it lead to?
receptor; to the drugs effect
most receptors are mainly ____
proteins
upregulation
a lot of slots on receptor to bind
downregulation/resistant
no slots on receptor for drugs to bind
apoptosis
cell death
ligand
molecule that bind to receptor involved in chemical signaling
what are some examples of ligands
neurotransmitter, hormone, drug, messenger molecultes
hormone
natural substance that is produced IN the body and that influences the way the body grows or develops
xenobiotic
chemical compound that is FOREIGN to a living organism
i.e. acetometophin is not made by the body so its foreign
toxin vs toxicant
biologic (snake venom, botox(bacteria)) vs nonbiologic (led, pharma)
drugs that binds to and activate receptor
agonist
how tightly a drug binds to receptor
affinity
amount of drug necessary to elicit a response
potency
drugs ability to produce the maximal desired response
efficacy
what happens to the dose if there is higher potency
smaller effective dose
when determining a drugs usefulness, is potency or efficacy more important?
efficacy
equi-potency
relative doses of two drugs to get the same efficacy
full vs partial agonist
produces a full (100%) response vs partially activating receptor regardless the conc.
antagonist
bind to receptor but block activation
*competitive antagonist
compete with other drugs— binds to receptor and prevent binding by OTHER molecultes
allosteric antagonism
binds to allosteric site on receptor to prevent agonist action
AKA– binds to different site on receptor changing structure thus preventing other things from binding
chemical antagonism
binds directly to agonist
functional antagonism
indirectly inhibits physiologic actions of the agonist
ex: treating somebody with asthma and DM give steroids and insulin which have opposing effects on glucose
… interactions that fight with effect
reversible antagonists
readily dissociate from their target
–when drug is gone it goes back to normal fx
irreversible antagonists
form a permanent, irreversible chemical bond with their receptor
–until body can produce new targets
what is the difference b/w competitive and noncomp antagonist
comp- agonist/antagonist CONC. determines effect.. a higher amt of agonist can reverse antagonist vice versa
noncomp-binds to receptor with STRONG affinity that receptor is no longer available to bind to agonist regardless of the conc.
some effects of opiods
analgesia, euphoria, resp depression, CNS depression, miosis
differ b/t high and low specificity
high- ONE type of receptor, limited toxicity ex (antibiotics)
low- MULT receptor activities and more adverse effects (chemotherapy)
explain racemic mixture
there’s a r./l. hand of drug (50/50 mixture)
-one enantiomer may either cause a therapeutic effect or a toxic effect..
pharm try to separate it to reduce side effects… essentially sell it for more $$$$ esp when finding omething new
what happens to the efficacy of the drug during down regulation
goes down
– less effect due to decreasing receptors
in order to retain effectiveness during down regulation…
have to increase dose
antagonist cause ____ and agonist cause _____
upregulation- too much blockage so body says to bring new cells for more open slots
downregulation- not enough spots due to too much activity
bioavailability
amt of drug that is ABSORBED through a given route
-IV is faster than oral
first pass effect
when drug is absorbed through GI, *liver metabolizes a portion prior to entering systemic cyrculation
prodrug
drug that must be activated before being physiologically active (liver)
volume of distribution
measure of apparent space in the body available to contain the drug
- how far drugs distribute into tissue vs stay in central blood supply
i. e. THC, high VD bc it stays in the fat
name routes of administration
- IV
- IM
- subcutaneous
- sublingual
- oral
- rectal
- inhalation
- transdermal
which ROA has the most rapid onset AND highest bioavailability
IV
which ROA has a large volume
Intramuscular (IM)
which ROA have 1st pass effect and which is most significant
oral***
- rectal
- transdermal
what’s meant by tritatable
continuous dosing
extravasation
drugs injected to tissue instead of vein
intraosseous
needle into bone marrow
-useful in emergent situations
what is a disadvantage of subQ
may cause pain or necrosis (anticoag)
what is an intrathecal ROA
injected in spinal cord- CSF, chemo
- has slow absorption
- placement is key
- headaches
enteric coating
resist stomach acids to later be absorbed and have a high bioavail.
who oversees all the drugs administered?
FDA
-food and drug admin.
phase 1 in clinical testing of medication
HEALTHY pts determining dose, safety, and kinetics (how its absorbed)
phase 2- testing medication
testing on pt with dz- determine efficacy
phase 3- medication
more ppl to further establish safety and efficacy
why can meds be so expensive
paying for the others that failed
how many years does it take till patent expires
20 years
bioequivalence
when 2 different drugs contain same active ingredients and are identical in strength/conc., dosage form, and ROA
ex: same drug diff manufacturers, generic
contact dependent (signaling)
cells must be direct contact
paracrine signaling
signals are released into space but rapidly taken by other cells or destroyed by enzymes
synaptic signaling
very specific and very rapid delivery - neurotransmitters
endocrine signaling
slow and nonspecific
-via bloodstream by hormones
digoxin
used for arrhythmia and congestive heart failure
three cell surface binding vs one intracellular
-ion channels
-g-coupled
-enzyme linked
and intracellular: (thyroid/steroid)
