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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

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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

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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

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4
Q

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

A

signal transduction pathway

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5
Q

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

A

drug receptors
(pharmacodynamics)

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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

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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

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8
Q

what did Paul Erlich discover

A

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

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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

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10
Q

what properties are important for selectivity

A

size
shape
charge
atomic composition

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11
Q

true or false

receptors mediate the action of agonists but not antagonists

A

FALSE - both.
both need to bind to the receptor

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12
Q

true or false

all receptors are proteins

A

FALSE - most receptors are proteins

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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)

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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

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15
Q

true or false

enzymes are receptors

A

true

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16
Q

true or false

enzymes are receptors that may be inhibited or activated by drugs

A

true, but inhibit is more common

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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)

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18
Q

give an example of how transport proteins can be drug receptors

A

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

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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

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20
Q

what is the receptor for colchicine

A

tubulin (a structural protein)

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21
Q

what is the receptor for methotrexate

A

DHFR (enzyme)

dihydro folate reductase

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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

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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

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24
Q

what is an “idealized” system

A

in vitro

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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

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26
Q

what is EC50

A

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

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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”

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28
Q

what is Emax

A

the maximal response that can be produced by a drug

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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

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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

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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

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32
Q

KD characterizes the receptor’s ______

A

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

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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)

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