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PHA112 > Drug Receptor Concepts > Flashcards

Drug Receptor Concepts Flashcards

1
Q

what is pharmacology?

A

study of interaction between drugs + living body

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2
Q

what is pharmacokinetics?

A

study of how body deals with/handles drugs

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3
Q

what is pharmacodynamics?

A

study of effects of drugs on living body + how effects = produced

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4
Q

what is pharmacotherapeutics?

A

study of use of drugs in treatment + prevention of disease

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5
Q

what are the 2 types of drug action?

A
  • non specific

- specific

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6
Q

non-specific drug action

A
  • some drugs act in simple physical/chem way (e.g. osmotic diuretics, antacids + chelating agents)
  • lack specific structure - activity relationship
  • needs large doses of drug for effect
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7
Q

specific drug action

A
  • most drugs act in highly specific way - e.g. phenylephrine, salbutamol, atropine, digoxin
  • interact with/bind to specific macromolecular/ cellular targets in body (receptors)
  • show clear cut structure -activity relationship
  • produce effects at v low doses
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8
Q

what is the drug receptor concept?

A

most drugs produce their biological effects by interacting with specific macromolecules in body called receptors

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9
Q

what is a receptor?

A

specialised component of cell/organism that interacts with drug + initiates chain of biochem events leading to drugs observed effects

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10
Q

what are drug receptors mainly?

A

protein / glycoprotein mol

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11
Q

give examples of drug receptors located on cell membrane?

A
  • atenolol
  • chlorphenamine
  • cimetidine
  • codeine
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12
Q

give examples of drug receptors located on inside of cell?

A
  • oestrogen
  • testosterone
  • vitamin D
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13
Q

what are the different types of drug targets / receptors?

A
  • classical - neurotransmitter, hormones
  • ion channels - lidocaine, diazepam, amiodarone
  • enzymes - NSAIDs, statins, ACE inhib
  • carrier/transport proteins - PPIs, digoxin, SSRIs
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14
Q

what law is the drug-receptor interaction governed by?

A

law of mass action

can relate drug conc + effect to fraction of receptors occupied

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15
Q

what do a drug + receptor interacts to form and how?

A

D-R complex

via reversible chemical interaction

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16
Q

what is the lock and key relationship based on?

A

selectivity of drug

  • chem selectivity
  • biological / tissue selectivity
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17
Q

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

A
  • conc of drug in biophase

- equilib dissociation constant (Kd) for d-r complex

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18
Q

what are the assumptions of the receptor occupancy theory?

A
  • drug effect = proportional to FRACTION of receptors occupied
  • max drug effect (Emax) happens when ALL receptors in systems = occupied
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19
Q

what are the possible outcomes of a drug-receptor interaction?

A

drug may mimic natural, endogenous chemical messenger —> prod same effect as natural chemical messenger (AGONIST)

drug may block access of natural, endogenous chemos messenger to receptor site —> prod no effect (ANTAGONIST)

drug may bind to site near binding site near binding site for natural, endogenous chem messenger + influence its binding —> inc + dec effect of chem messenger (ALLOSTERIC MODULATOR)

drug may bind to site normally occupied by natural, endogenous chemical messenger —> produce opposite effect to chem messenger (INVERSE AGONIST)

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20
Q

what does an agonist drug to?

A

produces same effect as natural chemical messenger

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21
Q

what does an antagonist do?

A

produces no effect

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22
Q

what is an allosteric modulator?

A

inc/dec effect of chemical messenger

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23
Q

what is an inverse agonist drug?

A

produce opposite effect to chem messenger

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24
Q

what do agonist and antagonist drugs both have?

A

affinity for their receptors

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25
Q

what is affinity?

A

measure of probability that drug mol = interact with receptor to form d-r complex

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26
Q

what is affinity measured by?

A

Kd of drug

affinity = 1/Kd

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27
Q

differentiate between agonist drugs and antagonist drugs?

A

agonist drugs have efficacy whilst antagonist drugs have NO efficacy

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28
Q

what is efficacy?

A

measure of biological effectiveness of drug-receptor complex

also = measure of ability of d-r complex to couple/ transduce drug binding into biological response

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29
Q

what may efficacy (e) be?

A

0, low + v. high

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30
Q

what is an agonist?

A

drug that binds to its receptor, activates receptor + elicits biological response

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31
Q

what are the 2 types of agonist?

A
  • full agonist

- partial agonist

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32
Q

what is a full agonist?

A

binds to its receptor + is capable of eliciting the max poss response from receptor system

has HIGH efficacy
e.g. dobutamine, salbutamol

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33
Q

what is a partial agonist?

A

binds to its receptor + is capable of eliciting LESS than max poss response from receptor system

intermediate efficacy (e)

reduces response elicited by full agonist

e.g. buprenorphine, oxymetazoline

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34
Q

what is an antagonist? (pharmacological)

A

drug that binds to its receptor but fails to activate receptor, + so fails to elicit a response

has efficacy of 0

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35
Q

an antagonist competes with…

A

agonist drug (or natural chem messenger) for binding to receptor

36
Q

where does an antagonists biological effect result from?

A

preventing agonist drug from binding to its receptor

e.g. atenolol, chlorphenamine, naloxone

37
Q

what is the ‘spare receptor’ / ‘receptor reserve’ concept?

A
  • exceptions to ‘receptor occupancy theory’
  • full agonists elicit max response WITHOUT full receptor occupancy
  • system has spare receptors
38
Q

what does the spare receptor concept enable?

A
  • economy of hormone / transmitter secretion

- allows low affinity drugs to elicit max poss response

39
Q

characteristics of the graded dose-response curve

potency

A

measures amount of drug needed to elicit specified response

  • reflected in location of D-R curve along dose axid
  • expressed as ED50 / EC50
  • clinically expressed as ABSOLUTE / RELATIVE potency
  • NOT critical characteristics

e.g morphine vs diamorphine

40
Q

what is maximal efficacy?

A

maximal response / effect produced by drug

41
Q

characteristics of graded dose-response curve

maximal efficacy

A
  • reflected as plateau in log D-R curve
  • MOST imp characteristic of drug

e. g. paracetamol vs morphine
- may = determined/limited by onset of adverse side effects

42
Q

characteristics of graded dose-response curve

slope

A
  • reflects magnitude of change in response with unit of change in dose
  • imp consideration under certain circumstances
43
Q

characteristics of graded dose-response curve

biological variability

A
  • DIFF responses to same dose of drug in DIFF people
  • DIFF responses to same dose of drug in SAME people
  • sources of variation in response: age, genes, gender, poly pharmacy, pathological state
44
Q

define drug antagonism?

A

interaction between 2 drugs so that the effect of 1 is diminished/completely abolished in presence of other

45
Q

what are the types of drug antagonism?

A
  • competitive (pharmacological/receptor)
  • non- comp
  • chemical
  • pharmacokinetic
  • physiological / functional
46
Q

competitive antagonism

A

agonist + antagonist drugs compete for same receptor binding site

  • antagonist binding reduces chance of agonist binding —> dec agonist effect
  • 2 subtypes, depending on nature of antagonist-receptor interaction
47
Q

what are the 2 subtypes pithing competitive antagonism?

A
  • reversible/surmountable

- irreversible/insurmountable

48
Q

reversible competitive antagonism?

A
  • antagonist + agonist bind REVERSIBLY to receptor
  • fraction of receptors occupied depends on drugs’ relative AFFINITIES + CONC
  • antagonism can = overcome by inc conc of agonist drug
49
Q

what are the 2 effects on the agonist log D-R curve for reversible competitive antagonism?

A
  • parallel shift to right

- no reduction in maximal response

50
Q

irreversible competitive antagonism?

A
  • antagonist drug binds IRREVERSIBLY to receptor (high affinity/cov bonding)
  • fraction of receptors = permanently unavailable for agonist drug binding
  • antagonist NOT OVERCOME by inc conc of agonist drug
51
Q

what are the 2 effects on the agonist log D-R curve for irreversible competitive antagonism?

A
  • reduction in slope of curve

- reduction in maximal response

52
Q

non-competitive antagonism?

A
  • antagonist drug DOESNT compete with agonist drug for same receptor binding site
  • antagonist drug may bind to diff site on receptor/interfere with response coupling
  • antagonism CANT = overcome by inc conc of agonist drug
53
Q

what are the 2 effects on the agonist log D-R curve for non-competitive antagonism?

A
  • reduction in slope of curve

- reduction in maximal response

54
Q

chemical antagonism?

A
  • direct interaction between agonist and antagonist drugs
  • ‘antagonist’ drug binds to/combines with active drug (agonist) in sol
  • active drug = inactive/unavailable to interact with target receptors
55
Q

what are the typical examples of chemical antagonism?

A
  • protamine vs heparin

- dimercaprol vs heavy metals (Cd, Pb)

56
Q

pharmacokinetic antagonism?

A

‘antagonist’ drug acts to reduce effective conc of active drug (agonist) at site of action

57
Q

what are the possible mechanisms for pharmacokinetic antagonism?

A
  • reduced absorption from GIT: ferrous salts vs tetracycline antibiotics
  • inc metabolic degradation: phenobarbitone vs warfarin
  • inc renal excretion:
    NaHCO3 vs aspirin
58
Q

physiological/functional antagonism?

A
  • interaction of 2 opposing agonist effects in single biological system —> cancelling out of each others effect
  • 2 drugs elicit OPPOSING responses by acting on diff receptors
59
Q

what are the typical examples of physiological/functional antagonism?

A
  • Ach vs noradrenaline (heart rate)

- glucocorticoids vs insulin (blood sugar levels)

60
Q

what is summation?

A

combined effect of 2 drugs elicits same overt response, regardless of mechanism of action = algebraic sum of individual effects

61
Q

what is additivity?

A

combined effect of 2 drugs, acts by same mechanism = to what is expected by simple addition of individual effects

62
Q

what is synergism/potentiation?

A

conjoint effect of 2 drugs = greater than algebraic sum of individual effects

63
Q

what may a synergist act to do?

A
  • inc conc of other drug at receptor sites: tyramine + MAO inhib
  • inc responsiveness of other drugs receptor - effector protein: benzodiazepines + GABA (gaba A receptor)
64
Q

what does the binding of GABA cause?

A

Cl- ion channels to open —> hyperpolarisation of cell

65
Q

what does the binding of GABA and benzodiazepine cause?

A
  • entry of Cl- hyperpolarises the cell —> more difficult to depolarise —> reduces neural excitability
  • binding of GABA = enhanced by benzodiazepine —> greater entry of Cl- ions
66
Q

variation in drug responsiveness - scope?

A
  • inter patient variation

- intra patient variation

67
Q

variation of drug responsiveness - poss consequences?

A
  • lack of efficacy

- unexpected side effects

68
Q

variation in drug responsiveness - poss mechanisms?

A
  • pharmacokinetic

- pharmacodynamic

69
Q

variation in drug responsiveness - poss types of variation?

A
  • qualitative

- quantitative

70
Q

variation in drug responsiveness - quantitive variations?

A
  • hyper - responsiveness

- hypo - responsiveness / tolerance

71
Q

variation in drug responsiveness tolerance?

A
  • innate vs acquired tolerance

- tolerance vs tachyphylaxis

72
Q

what is acquired tolerance?

A

acquired state of progressively dec responsiveness to drug as a result of prior repeated exposure to the drug / another drug with similar action

73
Q

what are the mechanisms for acquired tolerance?

A
  • pharmacodynamic
  • metabolic
  • exhaustion / depletion of mediators
  • physiological adaptation
74
Q

mechanism of acquired tolerance - pharmacodynamic?

A
  • receptor down regulation
    reduction in receptor density e.g. Beta 1 adrenergic receptor
  • receptor uncoupling
    uncoupling of receptors from effector systems e.g. Beta 2 adrenergic receptor
75
Q

mechanism of acquired tolerance - metabolic?

A
  • enhanced metabolism of drug
  • due to induction of metabolising enzymes
    e. g. alcohol, barbiturates
76
Q

mechanism of acquired tolerance - exhaustion/ depletion of mediators?

A
  • common with indirectly-acting drugs
  • due to depletion of endogenous stores of mediators of drugs action
    e. g. amphetamine, nitrates
77
Q

mechanism of acquired tolerance - physiological adaptation?

A
  • evoked compensatory / homeostatic mechanisms
  • blunts / cancels drugs effects

e.g. diuretics, nitrates

78
Q

what are the 2 types of clinical selectivity?

A

absolute + relative

79
Q

what 2 effects do u get?

A
  • therapeutic / desirable

- adverse/ undesirable/ side effects

80
Q

absolute vs relative selectivity?

A
  • no drug has one single specific effect

- produces spectrum of effects

81
Q

define relative selectivity?

A

degrees to which drug acts upon given site relative to all possible sites of interaction

82
Q

therapeutic vs undesirable effects?

A

undesirable effects may = minor/serious

83
Q

how may undesirable effects come about?

A
  • both effects mediated via same receptor effector mechanism - e.g. nitrates, insulin, warfarin
  • both effects mediated via identical receptor in diff tissues e.g. haloperidol, verapamil
  • both effects mediated via diff types receptors e.g. salbutamol, propranolol
84
Q

what is therapeutic index determined by?

A

ratio of toxic to therapeutic dose

85
Q

formula for therapeutic index?

A

median toxic dose (TD50) / median effective dose (ED50)

86
Q

what does therapeutic index provide a useful measure of?

A
  • margin of safety of drug
  • benefit to risk ratio of drug

e.g. penicillin vs warfarin

PHA112 (37 decks)

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