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1S Q2 Flashcards

1
Q

“In the presence of this antagonist, the potency and maximal efficacy of the antagonist is reduced no matter how much the dose of the antagonist is increased.”

a. chemical antagonism
b. competitive antagonism
c. non-competitive antagonism
d. physiologic antagonism

A

c

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2
Q

This type of antagonism produces less specific effects and is less easy to control.

a. chemical antagonism
b. competitive antagonism
c. non-competitive antagonism
d. physiologic antagonism

A

d

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3
Q

“Exemplified by the interaction between epinephrine and propranolol, a beta-blocker.”

a. chemical antagonism
b. competitive antagonism
c. non-competitive antagonism
d. physiologic antagonism

A

b

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4
Q

The effect of the antagonist can be reversed by increasing the concentration of the antagonist

a. chemical antagonism
b. competitive antagonism
c. non-competitive antagonism
d. physiologic antagonism

A

a

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5
Q

This intracellular second messenger activates Protein Kinase C:

a. cAMP
b. DAG
c. cGMP
d. IP3

A

b

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6
Q

Percentage of the population that responded at each dose is plotted against the log of the dose administered

A

Quantal dose-response relationship

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7
Q

This type of receptor is used by antidepressant drugs that targets norepinephrine and serotonin.

A

Transport proteins

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8
Q

In Quantal Dose Response Plots:

  1. ED50
    2.LD50
A

1<2

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9
Q

In the presence of spare receptors:

  1. Drug Dose to reach Bmax
  2. Drug Dose to reach Emax
A

1>2

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10
Q

Maximal efficacy (Emax):

  1. partial agonist
  2. full agonist
A

1<2

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11
Q

Margin of safety:
1. therapeutic index = 30
2. therapeutic index = 1.5

A

1>2

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12
Q

Response is decreased du to prolonged exposure to the drug

A

Tolerance

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13
Q
  1. Therapeutic index
  2. drug efficacy
A

No relation

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14
Q
  1. LD50
  2. drug safety
A

Directly proportional

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15
Q
  1. Dose to produce 50% of the maximal effect (EC50) 2. Efficacy
A

Directly proportional

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16
Q
  1. TD50
  2. Clinical efficacy
A

No relation

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17
Q
  1. TD50
  2. Drug safety
A

Directly proportional

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18
Q
  1. Dose to produce 50% of the maximal effect (EC50)
  2. Potency
A

Inversely proportional

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19
Q

This increases the phopholipase C activity in bombesin receptors.

A

Gq

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20
Q

This decreases the adenylyl cyclase in muscarinic cholinergic receptors

A

Gi

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21
Q

Potency of a drug:
1. ED50 = 40mg/kg
2. ED50 = 10mg/kg

A

1<2

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22
Q

Drug binding causes a conformational change resulting in the transient opening of a central aqueous channel:

a. Intracellular receptors
b. G protein coupled receptor
c. Ligand-gated ion channels receptors
d. Tyrosine kinase coupled receptor

A

c

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23
Q

Drug binding causes two receptor molecules to bind to one another (intracellular receptors)

A

Tyrosine kinase coupled receptor

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24
Q

Use a transmembrane signaling system with three separate components

A

G protein coupled receptor

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25
Q

“Involves activation of 2nd messengers such as diacylglycerol, IP3 & cAMP”

A

Tyrosine kinase coupled receptor

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26
Q

Drug response at Bmax:

  1. Full agonist + partial agonist
  2. Full agonist alone
A

1<2

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27
Q

Dose to produce 50% of the maximal effect (EC50):

  1. Full agonist + competitive antagonist
  2. Full agonist alone
A

1>2

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28
Q

Drug response at Bmax:

  1. Partial agonist
  2. Full agonist
A

1<2

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29
Q

Maximal efficacy (Emax):

  1. Full agonist alone
  2. Full agonist + noncompetitive antagonist
30
Q

This mediates the action of insulin and cortisol

a. regulatory proteins
b. enzymes
c. transport proteins
d. structural protein

31
Q

In the presence of spare receptors:

  1. Drug Dose to reach Emax
  2. Drug Dose to reach Bmax
32
Q

One drug opposes the effect of the other by binding at a different receptor and counteract its effect

a. chemical antagonism
b. competitive antagonism
c. non-competitive antagonism
d. physiologic antagonism

33
Q

Exemplified by the interaction between heparin and protamine sulfate

a. chemical antagonism
b. competitive antagonism
c. non-competitive antagonism
d. physiologic antagonism

34
Q
  1. EC50 2. drug safety
A

Directly proportional

35
Q

Used neurons for synaptic transmission.

a. Intracellular receptors
b. G protein coupled receptor
c. Ligand-gated ion channels receptors
d. Tyrosine kinase coupled receptor

36
Q

“Median effective dose (ED50), median toxic dose (TD50) & median lethal dose (LD50) are derived from this”

A

Quantal dose-response relationship

37
Q

This decreases the adenylyl cyclase in alpha-2-adrenergic receptors

38
Q
  1. Therapeutic window
  2. Drug efficacy
A

No relation

39
Q

This increases the adenylyl cyclase in beta adrenergic receptors.

40
Q

This opens potassium channels in the heart muscles.

41
Q

In Quantal Dose Response Plots:

  1. ED50
  2. TD50
42
Q

In the presence of spare receptors:

  1. Kd
  2. EC50
43
Q

This intracellular second messenger releases calcium from storage vesicles.

44
Q

Response intensity is diminished in a given dose of the drug

A

Hyporeactive Response

45
Q

Maximal efficacy (Emax):

  1. full agonist
  2. partial agonist
46
Q

Maximal effect:
1. full agonist + competitive antagonist
2. full agonist alone 1 = 2

47
Q

Transmits its signal across the plasma membrane by increasing transmembrane conductance

A

Ligand-gated ion channels receptors

48
Q

Receptors for lipid soluble drugs

A

intracellular receptors

49
Q

When activated, receptors dimerize and phosphorylate specific intracellular protein substrates

A

Tyrosine kinase coupled receptor

50
Q

In the presence of an antagonist, the dose-response curve of the agonist is shifted to the right but the maximal efficacy remains the same

a. chemical antagonism
b. competitive antagonism
c. non-competitive antagonism
d. physiologic antagonism

51
Q

Drug response at Bmax:

  1. full agonist alone
  2. full agonist + partial agonist
52
Q

Dose to produce 50% of the maximal effect (EC50):
1. full agonist alone
2. full agonist + competitive antagonist

53
Q
  1. ED50
  2. drug safety
A

Inversely proportional

54
Q
  1. kd
  2. drug affinity for the receptors
A

inversely proportional

55
Q
  1. kd
  2. drug safety
A

no relation

56
Q
  1. Therapeutic index
  2. drug safety
A

directly proportional

57
Q

This intracellular second messenger mediates the hormonal action for glycogenolysis in the liver.

58
Q

Response intensity is increased in a given dose of the drug.

A

Hypereactive Response

59
Q

The effect of the antagonist is insurmountable

a. chemical antagonism
b. competitive antagonism
c. non-competitive antagonism
d. physiologic antagonism

60
Q

Exemplifed by the interaction between atropine, a muscarinic antagonist and metoprolol

a. chemical antagonism
b. competitive antagonism
c. non-competitive antagonism
d. physiologic antagonism

61
Q

Maximal efficacy & potency are derived from this.

A

Graded dose-response relationship

62
Q

Cytoplasmic enzyme domain, which may be a serine kinase, or a guanylyl cyclase

a. intracellular receptors
b. G protein coupled receptor
c. Ligand-gated ion channels receptors
d. Tyrosine kinase coupled receptor

63
Q

The largest receptor family and are also called seven-transmembrane or serpentine receptors.

A

G protein coupled receptor

64
Q

Margin of safety:
1. therapeutic window = 150
2. therapeutic window = 10

65
Q

This intracellular second messenger mediates the hormonal action for water reabsorption in the kidney

a. cGMP
b. IP3
c. cAMP
d. DAG

66
Q

This intracellular second messenger mediates the hormonal action for water reabsorption in the kidney

a. intracellular receptors
b. G protein coupled receptor
c. Ligand-gated ion channels receptors
d. Tyrosine kinase coupled receptor

67
Q

The intensity and duration of action are often limited by a process called receptor down-regulation:

a. intracellular receptors
b. G protein coupled receptor
c. Ligand-gated ion channels receptors
d. Tyrosine kinase coupled receptor

68
Q

Response is diminished rapidly after administration of the drug

A

Tachyphylaxis

69
Q

Unusual response to a drug not seen in most of the patients

A

Idiosyncratic Response

70
Q

Margin of safety:
1. Therapeutic index = 50
2. Therapeutic index = 2

71
Q

This type of receptor is used by lipid lowering drug statins

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