Midterm 1 Flashcards by Danny Leapman

the action of a drug on an individual

pharmacodynamics

How well did you know this?

Not at all

Perfectly

substance used in the diagnosis, treatment, or prevention of an illness

drug

How well did you know this?

Not at all

Perfectly

anti-emitic, specific muscarinic acetylcholine receptor antagonist of vestibular pathway, decreases ACh input

scopolamine

How well did you know this?

Not at all

Perfectly

vestibular, sensory, emotional, chemoreceptors, GI tract are all things that project to what

vomition center

How well did you know this?

Not at all

Perfectly

the way botox achieves specificity

local administration

How well did you know this?

Not at all

Perfectly

the study of drug administration, absorbtion, distribution, action, and excretion

pharmacokinetics

How well did you know this?

Not at all

Perfectly

routes of administration

oral, IV, intramuscular, inhalation, topical, subcutaneous, intraperitonial, intracranial

How well did you know this?

Not at all

Perfectly

Problems with oral administration

acidic environment in stomach, first pass effect (liver metabolism often reduces efficacy, but not loarsitan)

How well did you know this?

Not at all

Perfectly

first pass effect

drug must enter bloodstream: portal vein - liver - drug metabolism. Both acidic stomach env. and liver metabolism can reduce function of drug

How well did you know this?

Not at all

Perfectly

works better after metabolism

loarsitan

How well did you know this?

Not at all

Perfectly

MEC (desired response)

minimum effective concentration (always exists)

How well did you know this?

Not at all

Perfectly

point at which drug exceeds threshold

onset of effect

How well did you know this?

Not at all

Perfectly

point of drug being toxic

MEC (adverse response)

How well did you know this?

Not at all

Perfectly

Difference between drug threshold and toxic threshold

therapeutic window

How well did you know this?

Not at all

Perfectly

Time it takes for half of drug to leave system

Half-life (T1/2)

How well did you know this?

Not at all

Perfectly

Repeated doses to achieve steady state leads to this curve shape

sigmoidal

How well did you know this?

Not at all

Perfectly

Fast onset, large volumes, sterility problem, must be hydrophilic

How well did you know this?

Not at all

Perfectly

Steady absorbiton, hydrophobic, sterility problems, sometimes irritating

Intramuscular

How well did you know this?

Not at all

Perfectly

Gaseous (volatile), fast onset, sometimes requires flame

Inhalation

How well did you know this?

Not at all

Perfectly

slow, steady absorption, only hydrophobic

Topical

How well did you know this?

Not at all

Perfectly

implantation of pellet, slow, steady absorption, sterility problems, removal problems

subcutaneous

How well did you know this?

Not at all

Perfectly

injection into abdomen, fast availability, sterility problem, used for lab rats

Intraperitoneal

How well did you know this?

Not at all

Perfectly

drug effectiveness/absorbtion graph

IV, IP, IM, oral(PO)

How well did you know this?

Not at all

Perfectly

directly to CNS, sterility problem, (epidurals)

Intracranial

How well did you know this?

Not at all

Perfectly

drug enters and exits body tissues

Equilibrium

Drug doesnt know where you want it to go

hydrophilic, hydrophobic, specific receptors, etc.

tissue drug has no effect in and gets trapped in, no receptors

drug reservoir

example of drug reservoir

adipose tissue

nonspecific assoiation, other drug reservoir that isnt drug reservoir, is reversible, amino acids attractive to drug

proteins

liver chemically alters drugs to make removal easier

metabolism

metaolized drug

metabolite

why is transformation from ph 2 to 7 necessary

make absorption possible, must be nonpolar to cross lipid bilayer

why weak bases are good oral candidates

protonation in stomach, becomes neutral

BBB is different in this way

tight junctions and astrocytic feet

R-CH2-CH3 -->(cytochrome P450) --> R-CH(OH)-CH3

oxidation

R-NO2 --> R-NH2

reduction

R-CO2R'-->esterases>R-CO2H+R'OH

hydrolysis

R-OH + R --> R-O-R'

conjugation

contains furanocoumarins which inhibit a P450 enzyme, increases levels of lipitor in bloodstream | can also block transporters in intestine which are responsible for uptake (allegra)

grapefruit juice

urination, sweat, exhalation, liver--bile

excretion

bifunctional role of receptor, one "thing" for which atropine and pilocarpine are competing in salivary glands (DATE, PERSON, THEORY NAME)

john langley (1878)- receptor theory

coined the term "receptor," lock and key metaphor (person and dates)

Paul Ehrlich (1854 - 1915)

molecules that bind receptors

ligands

cause a positive response (biological), can initiate second messenger response

agonist

binds with high affinity, but doesn't have biological effect (nothing turned on in cell), no second messenger pathway, blocks normal chemical binding, blocked cellular activity

antagonist

one example antagonist can be used for response

narcan for heroin overdose

stimulates adenylyl cyclase - takes ATP and forms cAMP, alters PKA, catalytic subunits run free and phosphorylate downstream targets

inhibits adenylyl cyclase

stimulates PLC - DAG-->PL(K?)C

couples directly to ion channels

how many transmembrane domains do G protein receptors have?

nicotine is agonist for this type of channel

ligand-gated ion channel

transporter: just takes one

uniporter

transporter: picks up one from inside, one from outside, and swaps them

antiporter

transporter: takes multiple things at once and moves them to other side of membrane

symporter

transporter: uses ATP

ATP-driven transporter

proteins which interact with DNA following binding of a ligand (e.g. estrogen)

Transcriptional activator

receptor where each monomer has half of the receptor sites, presence of ligand bring 2 monomers together, they phosphorylate each other, then phosphorylates downstream intracellular target

Tyrosine Kinase Receptor

Drug binding to receptor is:

reversible

computer runs water molecule over protein surface, this helps us determine:

protein shape

how much drug wants to get into and stay in binding pocket | "ability of drug to bind receptor"

affinity

4 factors that determine drug affinity

steric interactions, ionic bonds, hydrogen bonds, hydrophobic interactions (all reversible), covalent bonds rare

Concentration at which 50% of receptors are bound

Kd (affinity constant), logarithmic curve, smallest concentration that achieves Kd has highest affinity, Kd is inflection point

concentration of competitor at which we lose 50% of first drug binding

IC50

binding assay demonstration

once receptors are filled, more drugs wont bind

how fast drug associates with receptor

k1- forward rate constant

how long it takes drug to come off of receptor

k-1 - reverse rate constant

k-1/ k1

reflects affinity

ability of drug bound to receptor to induce intracellular activity

efficacy

intrinsic efficacy of 1

full agonist

intrinsic efficacy btw 0 and 1

partial agonist

intrinsic efficacy of 0

antagonist

regions responsible for making associations with drug - influences affinity

binding domain

region that interacts with drug that "turns on" receptor (conformational change)

activation domain

____ is a measure of how well a drug binds; ____ is a measure of how well a drug can produce desired effect

affinity, efficacy

dose response curves can tell you response to drug, but neither ___ or ____ specifically

affinity, efficacy

concentration of drug at which 50% of population exhibits a response after a certain period

EC50, lower EC50 is a better drug

receptor expression, ligand affinity, and intrinsic efficacy, all constitute:

drug effectiveness

receptor expression is not ___ within population, or even within people

constant

with sudden high concentrations of agonist, receptor becomes phosphorylated, inactivated, and internalized/sequestered

desensitization

with chronic levels of agonist, receptors become phosphorylated multiple times, inactivated, and internalized, having been tagged for degradation, B- arrestin involved

downregulation

administration of 2nd drug to allow re-sensitization of 1st drug's receptors

drug vacation

drug binding and biological response are ___ correlated

directly

Therapeutic index

TD50/ED50 (2 is not safe drug, doubling dose causes side effects in 1/2 of population

Therapeutic window

TD50 - ED50

3 categories of neurotransmitters of ANS

ACH, catecholamines (NE and E), and indolamines (serotonin)