Pharm Exam 1-1

Front 1

xenobiotics

Back 1

chemicals not synthesized by the body

Front 2

how do we limit the definition of a drug

Back 2

something not required for normal function

Front 3

3 reasons to use drugs

Back 3

treat
cure
prevent

Front 4

what the drug does to the body

Back 4

pharmcoDYNAMICS

Front 5

what the body does to the drug

Back 5

pharmcokinetics

Front 6

the study of drug safety?

Back 6

pharmcovigilance

Front 7

pharmacogenomics?

Back 7

variations in response due to genetic differences. build individualized medical care

Front 8

pharmacodynamics is all about..

Back 8

binding to receptors.. producing response through receptors

Front 9

receptors are defined as..

Back 9

proteins on or in cells that mediate the effect of the drug and bind with affinity and selectivity

Front 10

targets of drugs?

Back 10

receptors
enzymes
chemical or physical agents

Front 11

most all drugs use ___ to cause there effect

Back 11

receptors

Front 12

what drug works by chemical or physical agents?

Back 12

antacids (changing ph)
osmotic diuretics (large molecules increasing urine out put)

Front 13

hides within membranes

Back 13

hydrophobic

Front 14

what is rally important in the proteins in terms of its function

Back 14

shape

Front 15

most drug interactions are through ___ forces

Back 15

VDW

Front 16

IMPACT OF A drug binding to a receptor?

Back 16

the interaction causes a change in shape in the receptor.. which causes a change in function

Front 17

name the 4 types of receptors

Back 17

ion
g protein
enzymatic cystolic domains
intracellular

Front 18

ion channels

Back 18

multi subunits making a pore that allows selective things in and out (GABA A)

Front 19

MOST NUMEROUS RECEPTOR TYPE

Back 19

g protein

Front 20

g protein receptor the parts..

Back 20

has a extracellular domain that interacts with the drug...then has a 7 trans membrane spanning loop, then intracellular tail that goes with the g protein

Front 21

enzymatic cytosolic domains

Back 21

insulin receptor have a single trans-membrane domain. then intracellular they have some kind of enzymatic domain.

Front 22

intracellular receptors?

Back 22

steroid family receptors. (lipophillic things go right through)

Front 23

most drugs that use intracelluar receptors..

Back 23

have very slow effects cause they work through transcription

Front 24

g protein receptor types 3

Back 24

ligand gated (something has to bind)
voltage gated
2nd messenger (ligand binds leading to changing and releasesing 2nd messanger system that will make a chnage)

Front 25

g protein subunit .. how does it work

Back 25

alpha binds gtp and it leaves the beta gamma to activate 2nd messenger

Front 26

g proteins that activate ca channels

Back 26

activate adenylyl cyclase,G stimulatory

Front 27

activate K+ channels and inhibit adenlyl cyclase

Back 27

G inhibitory

Front 28

normal cell has high___ on the outside

Back 28

na+

Front 29

activates phospholipase c pathway? inhibits ca channels?

Back 29

G q

G o

Front 30

integrating second messenger systems?

Back 30

the cell can get bound by to different things causing 2 opposing second messenger systems

Front 31

tachyphylaxis

Back 31

repeated RAPID adim of the same dose of a drug results in a reduced effect of the drug over time
(rapid response do to repeated exposure)

Front 32

desensitization

Back 32

decreased ability of a receptor to respond to stimulation by a drug

Front 33

inactivation

Back 33

a total loss of the receptors ability to respond

Front 34

homologous desensitization?
heterologous desensitization?

Back 34

-decrease response at a single type of receptor

- several receptors decrease in their response

Front 35

receptor become refractory when..

Back 35

after the receptor is stimulated there is a period when the drug cant respond to anything else

Front 36

down-regulation

Back 36

repeated or persistent drug receptor interaction the receptor will be taken up and sequestered.

Front 37

kd=?

Back 37

rate of dissociation K off / rate of of combining Kon

Front 38

Kd is ..?

Back 38

different for each drug. concentration of the drug that binds 50% of the receptors

Front 39

affinity (kd)

Back 39

attractiveness of the drug

Front 40

lower the Kd..

Back 40

the higher the affinity

Front 41

saturation

Back 41

when adding more drug wont do anything

Front 42

graded dose curve? whats the EC50

Back 42

effects of various doses of a drug.
effect/ effect maximum

Front 43

Quantal dose response curves

Back 43

shows response in a population.

Front 44

effective dose 50

Back 44

when 1/2 the pop responds therapuetically

Front 45

TD50

Back 45

toxic dose for 50 % of population

Front 46

LD50

Back 46

50% of pop would die

Front 47

do antagonists have any intrinsic acity?

Back 47

no cause the will bind to receptor and nothing will happen in the receptor

Front 48

receptor antagonists..

Back 48

when something binds to the receptor and blocks effect

Front 49

nonreceptor antagonists

Back 49

when the antagonism occurs through something not using the receptor at all

Front 50

receptor antagonist 2 types

Back 50

binds to the receptor active site antagonist

or if it binds to another part of the receptor its a allosteric antagonist

Front 51

if the antagonists binds to the active site it can be..

Back 51

competitive antagonist- meaning its reversible... if i add more agonist it will be out done and the agonists will win.

irreversible

Front 52

active site antagonist that's irreversible

Back 52

noncompetitive active site antag. even with more "agonist" added it wont "win" cause the antag isnt coming off

Front 53

allosteric binding types of antagonisms

Back 53

both are noncomp allosteric antagonism. reversible or non reversible

Front 54

when a drug binds a receptor its called

Back 54

intrinsic activity (efficacy)

Front 55

pure antagonists has..? full agonist has?

Back 55

no intrisic activity (efficacy)

1

Front 56

intrinsic activity aka..

Back 56

efficacy

Front 57

potency=

Back 57

ec50
concentration when its half max effective

Front 58

what sit mean if ec50 occur at lower dose

Back 58

your drug is more potent

Front 59

max response in the presence of comp. antag.

Back 59

the same max response just requires more drug (will shift the EC50)

Front 60

irreversible noncomp antagonist... ec50 (potency) and max response?

Back 60

ec50 hasn't changed but the max response has lowered (cause it takes up receptors and doesn't let anyone else bind)

Front 61

shifts the ec50 but not max response

Back 61

agonist + comp antag

Front 62

shifts max effect but not potency

Back 62

noncomp antag + agonist

Front 63

inverse agonist

Back 63

prevents base line activity

Front 64

spare receptors

Back 64

ec50 occurs before you saturate 50% of the receptors usually do to amplification. getting max response before the receptors are fully saturated
ec50 < KD

Front 65

binding? effect?

Back 65

kd
ec50

Front 66

only high concentrations of the spare receptors..

Back 66

it will look like a true noncomp. antagonist. at low doses it looks like comp. antagonists

Front 67

therapeutic window

Back 67

Toxic 50 / effective dose 50

Front 68

who will associate with alipid bilayer

Back 68

hydrophobic

Front 69

inverse agonist

Back 69

agonist that prevents a receptor from reverting to spontaneous activation

Front 70

agonist with intrinsic activity less than 1

Back 70

partial agonist

Front 71

dose response curve for a population

Back 71

quantal

Front 72

activated by alpha gtp subunit

Back 72

effector molecule

Front 73

sigmoid drug receptor binding curve is on a _____ plot

Back 73

semilogarithmic

Front 74

pharmcovigiilance deals with this aspect of pharm

Back 74

toxicology

Front 75

intrinsic activity =

Back 75

efficacy