Brainscape's Knowledge GenomeTM

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


See full index

PH112 > Drug Receptor Concenpts ✅ > Flashcards

Drug Receptor Concenpts ✅ Flashcards

1
Q

what are the two drug taking processes?

A

the action of the drug on the body
action of the body on the drug

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

what are the branches of pharmacology?

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

how do drugs act?

A

interact with biological systems in ways that mimic or affect the natural chemical messengers or processes of the body.

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

what are the two types of drug action?

A

specific
non specific

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

what is non-specific drug action?

A

act in a simple physical or chemical manner
lack any specific structure-activity
relationship
requires large doses of drug for effect

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

what is specific drug action?

A

act in a highly specific manner
interact with or bind to specific macromolecular or cellular targets (receptors)
show clear cut structure-activity relationship
produce biological effects at very low doses

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

what is a receptor?

A

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

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

drug receptor molecules?

A

protein or glycoprotein

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

where are the drug receptors located?

A

cell membrane (e.g. atenolol) or inside the cell (oestrogen).

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

what are the two types of receptors? (protein or glycoprotein)

A

GABA a receptor
B1-adrenergic receptor (B = beta sign 1 is small one bottom, - is minus.)

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

what are the muplitiple types

A

‘classical receptors’
‘ion channels’
enzymes
carroer or trasnport proteins

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

what are classical receptors?

A

regulatory protein or binding sites for endogenous or natural chemical messengers, such as neurotransmitters and hormones.

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

what law is the drug-receptor interaction governed by?

A

Law of Mass Action

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

how do drugs and receptors interact?

A

complementary fit between the drug molecule and the binding site on the receptor.
-drug and receptor interact to form a drug-receptor (D-R) complex via a reversible chemical reaction.

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

how can we relate drug concentration and biological effects?

A

to the fraction of receptors occupied by the drug

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

lock and key relationship

A

basis of the selectivity of drug action
chemical selectivity
biological or tissue selectivity

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

drug-receptor interaction

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

what is the fraction of receptors occupied by the drug a function of?

A
  • concentration of drug in the biophase
  • the equilibrium dissociation constant (Kd) for drug-receptor complex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

the curve of the drug concentration-receptor occupancy curve

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

what are the assumptions of the ‘receptor occupancy theory’

A

drug effect is proportional to the fraction of receptors occupied.
maximum drug effect (Emax) occurs when all receptors in the system are occupied by the drug.

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

drug concentration-effect curve

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

Log drug concetration-effect curve

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

how does an agonist drug work? (drug-Receptor interaction 1)

A

drug may mimic a natural, endogenous chemical messenger → produce the same effect as the natural chemical messenger.
‘a drug that binds to its receptors, activates the receptor, and elicits a biological response’

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

how does an antagonist drug work? (Drug-receptor interaction 2)

A

the drug may ‘block’ the receptor e.g. prevent the natural chemical messenger from binding → this produces no effect.

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

how does an allosteric modulator work? (drug-receptor interaction 3)

A

drug may bind to a site near the binding site for a natural, endogenous chemical messenger and influence its binding. → or increase or decrease the effect of the natural chemical messenger.

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

how does an inverse agonist drug work? (drug-receptor interaction 4)

A

the drug may bind to the site normally occupied by a natural, endogenous chemical messenger.→ produce an opposite effect to the natural chemical messenger.

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

drug-receptor interaction diagram (last two names are different to what has been taught)

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

what is the basic similarity between agonist and antagonist drugs?

A

both have an affinity for their receptors.

29
Q

what does affinity express?

A

the chances of the drug binding to ist receptors.

30
Q

how is affinity measured?

A
31
Q

what is the basic distinction between agonist and antagonist drugs?

A

agonist drugs have efficacy whereas antagonist have no efficacy

32
Q

what is efficacy?

A

the measure of the ability of the drug-receptor complex to couple or transduce the drug binding into a biological response.

33
Q

how can efficacy be measured?

A
34
Q

Full agonist description

A
35
Q

Partial agonist description

A
36
Q

Antagonist description

A
37
Q

how does an antagonist drug produce its biological ‘effect’

A

competes with agonist drug/natural chemical messenger to bind to receptor
preventing the agonist drug/natural chemical messenger from binding to its receptors

38
Q

what is the spare receptor/receptor reserve theory?

A

the exception to the receptor occupancy theory

full agonists may elicit a maximum response without full receptor occupancy. these are known as spare receptors or receptor reserves.

39
Q

what is the spare receptor/receptor reserve theory?

A

the exception to the receptor occupancy theory

full agonists may elicit a maximum response without full receptor occupancy. these are known as spare receptors or receptor reserves.

40
Q

what does the spare receptor/receptor reserve concept enable?

A

the economy of hormone/transmitter secretion

allows low affinity drugs to elicit maximum possible response.

41
Q

graded dose response curve

A
42
Q

what are the characteristics of the graded dose-response curve

A

potency
maximal efficacy
slope
biological variability

43
Q

the potency for graded dose-response curve

A

amount of drug needed to elicit response
D-R curve of graded dose curve
clinically expressed as absolute or relative potency
experimentally expressed as ED50 or EC50 (numbers are small)
not a critical aspect of the drug

44
Q

potency rate

A
45
Q

the maximal efficacy for dose-response curve

A

maximal result/effect produced by the drug
the high curve on the grade-response curve
a most important characteristic of the drug
maximum efficacy may be determines or limited in clinical practise due to adverse effects

46
Q

the slope for dose-response curve

A

reflects magnitude of change in response per unit of drug
may be important to consider in clinical practise under certain circumstances.

47
Q

biological variability for dose-response cruve

A

different responses to same dose of drug to different people/same person
there are different sources of variation for drug response

48
Q

what are the possible sources of variation in drug reponse?

A

age
gender
genetic factors
pathological state
ploypharmacy

49
Q

drug antagonism

A

interaction between two drugs such that the effect of one is diminished or completely abolished in the presence of the other

50
Q

types of drug antagonism

A

competitive antagonism (pharmacological/receptor)
non competitive antagonism
chemical antagonism
pharmacokinteic antagonism
physiological or fcuntional antagonism

51
Q

competitive antagonism

A

agonist and antagonist drug compete for same receptor binding site
the binding of the anatgonist reduces the binding of the agonist binding which reduces the effect of the agonist
depending in nature of antagonist receptor intercation there are two subtypes of competitive antagonism; reversible or surmountable or ireversible or insurmountable.

52
Q

reversible competitive antagonism

A

agonist and antagonist drug binds reversibly to the receptor
fraction of receptors occupied depends on the two drugs relative receptor affinities and concentrations.
antagonism can be overcome by increasing the concentration of the agonist drug. leads to two effects on the agonist lod D-R curve when in the presence of the antagonist drug. this includes a parallel shift to the right and no reduction in the maximal response.

53
Q

irreversible competitve antagonism

A

antagonist drug bins irreversibly to the receptor (due to high effinity or covelant bonding)
fractions of receptors may be permanently unavailable for agonist drug binding
antagonism cannot be overcome by increasing the agonist drug concentration
leads to two effects on the agonist log D-R curve (in the presence of an effective dose of the antagonist drug). this includes a reduction in the slope of the curve and a reducton in the maximal response.

54
Q

non competitive antagonism

A

antagonist drug does not compete with an agonist drug for the same receptor-binding site
antagonist drug may bind to a different site on the receptor or may interfere with response coupling
antagonism cannot be overcome by increasing the agonist drug concentration
leads to two effects on the agonist log D-R curve (in the presence of an effective dose of the antagonist drug) this includes a reduction in the slope of the curve and a reduction in the maximal response)

55
Q

chemical antagonism

A

results from direct interaction between antagonist and agonist drug
antagonist binds to/ combines with ‘active’ agonist drug in the solution. the active drug is then rendered inactive or unavailable to interact with its target receptors.
examples, include protamine vs heparin and dimercaprol vs heavy metals (Cd, Pb)

56
Q

pharmacokinetic antagonism

A

antagonist drug works to reduce the effective concentration of the ‘active’ agonist drug at its site of action
possible mechanisms of this include (use slide to add examples)

57
Q

physiological/ functional antagonism

A

interaction of two opposing agonist effects in a single biological system. they cancel out each other’s effects.
two drugs elicit opposing responses by acting on different receptors
Examples include; acetylcholine vs noradrenaline, glucocorticoids vs insulin

58
Q

Summation

A

when the combine effect of two drugs which ellicit the same overt response, reagardless of theur mechanism of action, is equal to the algebraic sum of their individual effects.

59
Q

Additivity

A

when the combined effect of two drugs, which act by the same mechanism, is equal to that expected by simple addition of their individual effects.

60
Q

synergism or potentiation

A

when the conjoint effect of two drugs is greater than the algebraic sum of their individual effects
synergist may act to; increase the concentration of the other drug at its receptor site or increase the responsiveness of the other drug receptor-effector protein.

61
Q

variation in drug responses

A

scope:
interpatient variation
intrapatient variation

possible consequences
lack of efficacy
unexpected side effects

possible mechanisms
Pharmacokinetic
Pharmacodynamic

possible types of variation
qualitative variations
Quantitative variations; hyperresponsiveness/hypo responsiveness or tolerance

tolerance
innate vs acquired tolerance
tolerance vs tachyphylaxis (rapidly diminishing reponse to successive doses of drug)

62
Q

acquired tolerance

A

’an acquired state of progressively decreasing responsiveness to a drug as a result of prior or repeated exposure to the drug or another drug with a similar action’
there are different mechanisms to this; pharmacodynamic, metabolic, exhaustion/depletion of mediators, physiological adaptation

63
Q

mechanism of acquired tolerance - pharmacodynamic

A

receptor ‘down-regulation’. this is where there is a reduction in the receptor density.
receptor ‘uncoupling’. this is where the receptors uncouple from their effector systems.

64
Q

mechanism of acquired tolerance - exhaustion/ depletion of mediators

A

common with indirectly-acting drugs
due to the depletion of the internal stores of mediators of the drugs action e.g. amphetamine, nitrates.

65
Q

mechanism of acquired tolerance - physiological adaptation

A

Brings about a compensatory or homeostatic (A state of balance among all the body systems needed for the body to survive and function correctly) mechanism. e.g. diuretics, nitrates.

66
Q

clinical selectivity - absolute vs relative selectivity

A

no drug has only one single, specific effect
drugs produce a spectrum of effects, hence ‘relative’ not ‘absolute’ selectivity of drug action.
relative selectivity is known as the degree to which a drug acts upon a given site relative to all possible sites of interaction.

67
Q

clinical selectivity - therapeutic vs undesirable/side effects

A

drug effects split into therapeutic and undesirable
undesirable effects may be minor or serious.
both effects may come about via same receptor-effector mechanism. e.g. nitrates, insulin, warfarin
both effects may be mediated via identical receptors located in different tissues. e.g. haloperidol, verapamil.
both effects may be mediated via different types of receptors. e.g. slbutamol, propranolol

68
Q

clinical selectivity - the concept of therapeutic index

A

determined by the ratio of toxic to a therapeutic dose.
therapeutic index = median toxic dose (TD50) / median effective dose (ED50)
this provides a useful measure of the margin of safety of drug and the benefit-to-risk ratio os drug. e.g. penicillin vs warfarin.

PH112 (17 decks)

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