Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology Midterm (edit) > Lecture 2 Part 1 > Flashcards

Lecture 2 Part 1 Flashcards

1
Q

therapeutic and/or toxic effects of drugs result from what?

A

their interactions with molecules within patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

true or false

all drugs act by associating with specific receptors (macromolecules) in ways that alter the receptor’s biochemical or biophysical activities

A

FALSE

most, but not all

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

“the component of a cell or organism that interacts with a drug and initiates the chain of biochemical events leading to the drug’s observed effects”

A

drug receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the “chain of biochemical events” that occurs when the receptor interacts with the drug

A

signal transduction pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what has become the central focus of investigation of drug effects and their mechanism of action?

A

drug receptors
(pharmacodynamics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what 2 people observed things that made drug receptors the central focus of investigation of drug effects/mechanism of action

A

John Langley
Paul Erlich

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what did john langley notice

A

Curare did not prevent the electrical stimulation of muscle contraction, but DID block contraction that was triggered by nicotine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what did Paul Erlich discover

A

some synthetic organic agents had anti-parasitic effects while other agents didn’t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

name 4 ways in which the receptor has important practical consequences for the development of new drugs and therapeutic decisions

A

-receptors are sites of binding for drugs

-receptors are responsible for selectivity of drug action

-receptors mediate the actions of both AGONISTS AND ANTAGONISTS (both need to bind)

-receptors determine the quantitative relationships between dose/concentration of a drug and pharmacological effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what properties are important for selectivity

A

size
shape
charge
atomic composition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

true or false

receptors mediate the action of agonists but not antagonists

A

FALSE - both.
both need to bind to the receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

true or false

all receptors are proteins

A

FALSE - most receptors are proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the BEST CHARACTERIZED drug receptors?

A

regulatory proteins that mediate the actions of endogenous chemicals signals

(like neurotransmitters, hormones, and autacoids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

besides regulatory proteins that mediate actions of endogenous chemicals, name 3 other classes of proteins that have been clearly identified as drug receptors

A

-enzymes
-transport proteins
-structural proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

true or false

enzymes are receptors

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

true or false

enzymes are receptors that may be inhibited or activated by drugs

A

true, but inhibit is more common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

give an example of an enzyme that is a receptor for a drug

A

DHFR (dihydrofolate reductase) is the receptor for methotrexate (antineoplastic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

give an example of how transport proteins can be drug receptors

A

the receptor for cardioactive digitalis glycosides = Na+/K+ ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how can structural proteins function as drug receptors

A

tubulin = protein involved to maintain cellular integrity.

tubulin = receptor for colchicine – an anti-inflamm agent for gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the receptor for colchicine

A

tubulin (a structural protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the receptor for methotrexate

A

DHFR (enzyme)

dihydro folate reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

when is the relationship between dose and response potentially quite complex? when is it simple and can be described with mathematical precision

A

complex - when administered to a human

simple - in vitro studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

in intact patients or animals, the responses to low doses of drug usually ________ in proportion to dose.

however….

A

increases in direct proportion

as the dose continues to increase, the response increment diminishes and doses can finally be reaches at which no further increase in response can be achieved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is an “idealized” system

A

in vitro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

in idealized/in vitro systems, how is the relationship between drug concentration (C) and effect (E) described?

A

by a hyperbolic curve.
equation:

E = Emax * C / C + EC50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is EC50

A

the concentration of drug at which HALF OF MAXIMAL response is observed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

true or false

EC50 is 50% of the response

A

false – doesn’t fit if it’s a partial agonist

should be - “Half of maximal response” or “drug conc that produces half of maximal effect”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is Emax

A

the maximal response that can be produced by a drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the formula for the relation between bound and unbound drug?
explain

A

B = Bmax * C/ C + KD

B = drug bound to receptors
Bmax = total conc of receptor sites
C = conc of unbound drug
KD = equilibrium dissociation constant, represents the conc of FREE DRUG at which half-maximal binding is observed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

explain what KD is

A

equilibrium dissociation constant

represents the concentration of FREE DRUG at which HALF MAXIMAL BINDING is observed

characterizes the receptor’s affinity for binding the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

if KD is high, what does this say about binding affinity

A

LOW

bc KD represents the concentration of FREE DRUG at which half maximal binding is observed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

KD characterizes the receptor’s ______

A

AFFINITY for binding the drug (RECIPROCAL - meaning the higher the KD the lower the affinity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

true or false

when a receptor is occupied by an agonist, the resulting conformational change is the only step required to produce a pharmacological effect

A

FALSE

this is the first of many steps.

there is a transduction process called COUPLING

34
Q

the efficiency of receptor occupancy-response coupling is partially determined how?

A

by the initial conformational change in the receptor

35
Q

explain what spare receptors are

A

receptors are “spare” when the maximum response can be obtained by an agonist at a concentration that DOES NOT RESULT IN FULL OCCUPANCY OF THE AVAILABLE RECEPTORS

36
Q

TRUE OR FALSE

spare receptors are different from nonspare receptors

A

false - they’re the exact same

the drug (agonist) is just very efficient bc it is able to produce a full response without occupying all of them

37
Q

true or false

spare receptors are not hidden or unavailable

A

true – they’re there and available, just not needed

38
Q

true or false

when spare receptors ARE occupied, they can be coupled to a response

A

true

39
Q

true or false

KD is the concentration of the agonist at which half the receptors are bound

A

TRUE

40
Q

when the agonist binds to its receptor, it elicits what?
this enables what?

A

a change in receptor conformation enables the receptor to bind to and activate a TRANSDUCING MOLECULE

41
Q

In the case of having spare receptors, this means that there are less drug receptors than receptor-effector molecules

TRUE OR FALSE

A

FALSE – more drug receptors than receptor-effector molecules

42
Q

a cell has 4 receptors and 4 effectors

are there any spare receptors?

A

no.

43
Q

what can you say when an agonist is present in concentration EQUAL TO KD

A

50% of the receptors will be occupied.
half of the effectors will be activated, and thus a half maximal response will be produced

44
Q

an agonist is present at a concentration equal to KD.
the number of receptors increases 10 fold, and the total number of effectors remains constant.

are there any spare receptors?

A

yes - most of them are spare

this means that the drug is producing its maximal effect, even though only half of the available receptors are occupied

45
Q

true or false

when there is a situation with spare receptors, a low concentration of agonist is usually sufficient to produce a maximal response

A

true

46
Q

true or false

antagonists have affinity but no efficacy

A

true

47
Q

explain the effect of antagonists

A

they bind to the receptor but do not activate it.
they essentially BLOCK agonists (drugs/other endogenous regulatory molecules) from binding to and activating receptors

48
Q

how can antagonists be divided?

A

reversible antagonists (competitive inhibitor)

irreversible antagonists (non competitive inhibitor)

49
Q

true or false

reversible antagonists are also known as noncompetitive inhibitors

A

FALSE

competitive. they are competing for the same binding site.

therefore, increasing the concentration of the agonist can “reverse” the effects of the reversible antagonist

50
Q

explain the difference you would expect to see in a graph of agonist effect vs agonist concentration with:

-agonist
-agonist + competitive inhibitor

A

EC50 would be pushed to the right once the competitive inhibitor enters the picture

a higher dose of agonist would be needed to produce the normal agonist effects.

51
Q

true or false

EC50 is higher in the agonist than with agonist + competitive inhibitor

A

FALSE - higher with competitive inhibitor. more drug needed to produce same response

52
Q

true or false

for any fixed concentration of competitive antagonist, the emax will remain the same for the agonist

A

true – the concentration effect curve will just shift to the right and more dose will be needed to produce the SAME EMAX

53
Q

in a fixed concentration of competitive antagonist, a higher concentration of agonist is needed to produce a given effect (higher than the dose needed with just the agonist itself).

how can the ratio of these 2 agonist concentrations be estimated?

A

the SCHILD EQUATION

C’/C = 1 + ([I]/KI)

KI = dissociation constant of the antagonist

C’ = agonist concentration
I = concentration of antagonist

54
Q

true or false

in the presence of a fixed concentration of competitive antagonist, lower concentrations of agonist are required to produce a given effect

A

FALSE - higher concentrations are needed

55
Q

the degree of inhibition produced by a competitive antagonist is dependent on what?

A

THE CONCENTRATION OF THE ANTAGONIST

56
Q

true or false

in the case of a reversible antagonist, increasing the concentration would increase the inhibition of agonist

A

true

57
Q

what is a source of variability in clinical response to a competitive antagonist?

A

the concentration of agonist that is competing for binding to the receptors

the higher the concentration of the agonist, the better the response

58
Q

phenoxybenzamine

A

will destroy the receptor

59
Q

under circumstances where there is only agonist, only agonists can bind to the receptor.

when all the receptors are saturated, what do we see?

A

the maximal effect (EMAX)

60
Q

TRUE OR FALSE

antagonists bind to receptors, but do not activate those receptors

A

true

61
Q

true or false

when there is both agonist and antagonist, they can both bind to the receptor

A

true

62
Q

in the presence of competitive antagonists, the maximum effect will be diminished.
is there any way to over come this and still produce the maximum effect?

A

yes – by adding more agonist

63
Q

true or false

even at very low concentrations of reversible antagonist, the efficacy is still diminished

A

FALSE

if there is a lot of agonist, little amounts of competitive antagonist won’t affect the efficacy

at higher concentrations, efficacy will eventually start to decrease

64
Q

true or false

if there is a high enough concentration of competitive antagonist, ALL of the agonist may be displaced and replaced with antagonist

A

true

65
Q

true or false

in the presence of noncompetitive antagonist, increasing the concentration of agonist won’t do anything

A

true

66
Q

true or false

in the case of noncompetitive/irreversible antagonists, the antagonist’s affinity for the receptor may be so high that, for practical purposes, the receptor is UNAVAILABLE for binding of agonist

A

true

67
Q

give an example of irreversible antagonist

A

they produce covalent bonds with the receptor – irreversible effects (phenoxybenzamine)

68
Q

is EMAX decreased in the case of noncompetitive antagonists?

A

YES

at a certain point, when a lot of receptors are occupied by antagonist, the # of remaining unoccupied receptors may be too low for the agonist to elicit a maximal response (EVEN AT HIGH CONCENTRATION)

69
Q

true or false

with noncompetitive inhibitor, EC50 increases

A

false

it may remain the same

70
Q

true or false

covalent binding is an example of a competitive antagonist

A

FALSE – noncompetitive/irreversible

71
Q

in what case would a lower dose of irreversible antagonist still allow the achievement of a maximum response to the agonist?

A

if spare receptors are present

72
Q

when all receptors have been saturated with an irreversible antagonist, the addition of MORE AGONIST will NOT re-establish the response

TRUE OR FALSE

A

TRUE

73
Q

true or false

an agonist is unable to displace an irreversible antagonist, even at very high concentrations of agonist

A

true

74
Q

give a specific example of an irreversible antagonist and how it works

A

Phenoxybenzamine

an irreversible alpha adrenoceptor antagonist.
used to control hypertension caused by catecholamines released from a tumor of the adrenal medulla

75
Q

give the name for a tumor of the adrenal medulla.
what drug can be used to treat it?

A

pheochromocytoma

phenoxybenzamine – an irreversible alpha-adrenoceptor antagonist

76
Q

give an example of how the irreversible antagonist - phenoxybenzamine - provides a therapeutic advantage

A

even when the administration of phenoxybenzamine lowers, blood pressure will still be maintained, even when the tumor releases very large amounts of catecholamine

(bc it is an irreversible antagonist!!)

77
Q

explain a major therapeutic disadvantage of the irreversible antagonist - phenoxybenzamine

A

overdose can cause major issues

if the blockade of the alpha-adrenoceptor cannot be overcome, the excess effects of the drug must be antagonized “physiologically” – by using a pressor agent (anti hypotensive agent) that does NOT act via alpha receptors

catecholamines cannot displace phenoxybenzamine to combat its function bc it is an IRREVERSIBLE antagonist

78
Q

what happens when catecholamines bind to alpha adrenoceptors?

A

catecholamines act as agonists to stimulate an increase in blood pressure

79
Q

what happens in the case of a patient with pheochromocytoma

A

this adrenal medulla tumor will secrete excess catecholamines

these act as agonists to the alpha adrenoceptor and cause an excess increase in blood pressure

80
Q

true or false

catecholamines can displace phenoxybenzamine from the alpha adrenoceptors

A

FALSE

phenoxybenzamine is an irreversible antagonist and thus cannot be displaced by agonist

81
Q
A

Pharmacology Midterm (edit) (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions