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MEDI 202 - Genes To Community > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

What is pharmacodynamics?

A

The drug’s actions and effects on the body

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2
Q

How do drugs target certain organs and tissues?

A

By interacting with specific proteins like receptors

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3
Q

What is the process of signal transduction?

A

Drug (signal)
Membrane protein (receptors) (signal detector and transducer)
Effectors
Second messanger

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4
Q

What is a signal cascade effect and when does it happen?

A

It occurs when activated effectors produce second messengers that further activate other effectors.

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5
Q

What is the effect of receptor activation?

A

Induces cellular response that lasts several seconds to hours

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6
Q

What are ligands?

A

Biologically active substances that exert its action via a receptor.

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7
Q

What is the difference between hydrophilic and hydrophobic ligands?

A

Hydrophilic ligands: interact with receptors that are found of the cell surface

Hydrophobic ligands: enter cells through the lipid bilayers of the cell membrane ti interact with receptors found inside the cell.

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8
Q

What are receptors?

A

Proteins that transduce extracellular signals and intracellular responses

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9
Q

How can receptors be activated?

A

Endogenous agonists (hormones and neurotransmitters)
Exogenous agonists (drugs)

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10
Q

What does the activation of receptors lead to?

A

Biological response

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11
Q

What are the different kinds of receptors?

A

Ionotropic receptors, ligand receptors
G protein-coupled receptors
Enzyme-linked receptors
Intracellular recptors

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12
Q

What part of the ligand-gated channels contains the ligand binding site?

A

The extracellular portion

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13
Q

When do the ligand-gated channels open?

A

When the receptor is activated by a ligand

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14
Q

What does the ion conducted control?

A

Whether an action potential is generated or inhibited

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15
Q

What does stimulation of the nicotinic receptor by acetylcholine result into?

A

Sodium influx, because sodium is positively charged it generates an action potential.

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16
Q

Does sodium influx increase or decrease neuronal conduction?

A

It increases it

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17
Q

What results in a chloride influx?

A

Stimulation of the GABA receptor

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18
Q

What other effect does the stimulation of GABA have?

A

Hyperpolarization of neurons which decreases neuronal conditions

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19
Q

Which receptor type has the most rapid time response?

A

Ligand-gated ion channels

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20
Q

What kind of receptors are G-protein coupled receptors?

A

Transmembrane proteins

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21
Q

What does the extracellular domain of the GPCRs interact with?

A

Interacts with the ligand via ligand binding site

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22
Q

What does the intracellular domain of the GPCRs interact with?

A

Interacts with a G protein or effector molecule

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23
Q

What are G-proteins composed of?

A

Three different subunits: α, β, γ.

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24
Q

What does the α subunit bind to?

A

Guanosine diphosphate, inactive G protein.

Guanosine triphosphate, active G protein.

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25
Q

At what point does Gα bind to a GDP molecule?

A

At steady state

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26
Q

What happens if there is binding of an antagonist to the receptor?

A

GTP binding to Gα increases, causing dissociation of the Ga-GTP complex from the Gβγ complex.

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27
Q

How can the Gα complex and Gβγ complex interact with other cellular effectors?

A

Usually through an enzyme, protein, or an ion channel.

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28
Q

What happens to enzyme-linked receptors when activated?

A

They undergo conformational changes resulting in increased cytosolic enzyme activity

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29
Q

What structure do the most common enzyme-linked receptors possess?

A

Tyrosine-kinase activity

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30
Q

What happens if an enzyme-linked receptor is activated by an agonist?

A

The intrinsic tyrosine kinase activity causes autophosphorylation on the receptor itself.

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31
Q

What does the phosphorylated receptor do to other proteins?

A

It phosphorylates other proteins that subsequently activate other important cellular signals.

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32
Q

What does the cascade of enzyme-linked receptors lead to?

A

Multiplication of the initial signal

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33
Q

What is one of the characteristics of the ligands that bind to intracellular receptors? Why?

A

They need to have sufficient solubility, they need to be lipophilic to cross the membrane and interact with the receptor, since the receptors are completely intracellular.

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34
Q

What happens when intracellular receptors are activated by an agonist?

A

Intracellular receptors translocate to the nucleus, dimerizes before binding to transcription factors.

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35
Q

What is the function of the transcription factors?

A

Regulate gene expression.

36
Q

What is the rate of the pharmacological responses of intracellular receptors?

A

Slower in onset but longer in duration

37
Q

What are the two important features of signal transduction?

A

Amplify small signals
Protect cell from excessive stimulation

38
Q

What is one of the characteristics of GPCRs and enzyme-linked receptors? What does that mean?

A

Ability to amplify signal intensity and duration.

Only a fraction of the total receptors may need to be occupied to elicit a maximal response.

39
Q

What can one activated GPCR or enzyme-linked receptor do?

A

Activate many G proteins, multiplying the signal.
Each activated G protein then activates more receptors and persists for a longer duration.

40
Q

Are cellular responses short or long?

A

Short, seconds to minutes

41
Q

What is done to prevent the production of an intensified cellular response and potential damage to the cell?

A

Many molecular mechanisms evolve to deactivate signaling pathways and attenuate the sensitivity of the tissue

42
Q

What happens if a receptor is internalised?

A

Movement of receptors from plasma membrane to inside the cell, unavailable for further agonist interaction

43
Q

What does the magnitude of the drug effect depend on?

A

Drug concentration at the receptor site.

44
Q

What determines the concentration at the receptor site?

A

The dose of the drug administered and drug’s pharmacokinetic profile.

45
Q

What falls under the drug’s pharmacokinetic profile?

A

Rate of absorption, distribution, metabolism and elimination

46
Q

What is the dose-response curve?

A

As the concentration of the drug increases, the pharmacologic effect also gradually increases.

47
Q

When is the maximum effect of the drug reached?

A

When all the receptors are occupied which causes the plateau of the curve

48
Q

What is the dose-response curve described as?

A

SIgmodial hyperbola

49
Q

What does the pharmacological effect depend on?

A

Potency and efficacy

50
Q

What is potency?

A

A measure of the amount of drug necessary to produce an effect of a given magnitude.

51
Q

What usually determines the potency of a drug?

A

The concentration of the drug that produces 50% of the maximum effect (EC50)

52
Q

Compare drug with high potency to one with lower?

A

A drug of high potency evokes a given response at lower concentrations, while one with lower potency would evoke the same result but in higher concentrations.

53
Q

What is efficacy?

A

The magnitude of response a drug causes when it interacts with a receptor.

54
Q

What controls efficacy?

A

The number of drug-receptor complexes formed and the intrinsic activity of the drug.

55
Q

What is the intrinsic activity of the drug?

A

The ability to activate the receptor and cause a cellular response.

56
Q

What is maximal efficacy?

A

All receptors are occupied by the drug, so response should not increase even when concentration increases.

57
Q

What is the equation between drug concentration and receptor occupancy?

A

(DR)/(Rt) = ((D) / (Kd + D))
D = concentration of a drug
DR = the concentration of bound drug
Rt = the total concentration of receptors
Kd = the equilibrium dissociation constant for the drug from the receptor

58
Q

What determines the equilibrium dissociation constant for the drug from the receptor (Kd)?

A

The concentration of ligand required to occupy 50% of the total population of receptors.

59
Q

How is affinity determined?

A

Through the value of Kd

60
Q

What is affinity?

A

Strength of the interaction between a ligand and its receptors

61
Q

What does it mean when Kd is high?

A

Drug-receptor interaction is weak and the affinity of the ligand for the receptor’s binding site is low, and vice versa.

62
Q

What is an antagonist?

A

Bind to receptors with high affinity and produce zero intrinsic activity

63
Q

What happens to an antagonist in the presence of an agonist?

A

Antagonism may also occur either by blocking the drug’s ability to bind to the receptor or by blocking its ability to activate the receptor

64
Q

What are the different kinds of antagonists?

A

Chemical antagonist
Irreversible antagonist
Allosteric antagonist

65
Q

What is a chemical antagonist?

A

Interacts directly with the agonist and not the receptor

66
Q

What kind of antagonist binds covalently to the active site of the receptor?

A

Irreversible antagonist

67
Q

What is an allosteric antagonist?

A

It binds to a site other than the agonist-binding site and prevents the receptor from being activated by the agonist.

68
Q

What are the two kinds of irreversible antagonists?

A

Agonist alone
Agonist-antagonist

69
Q

What are the types of allosteric antagonists?

A

Agonist alone
Agonist - antagonist

70
Q

Will the presence of irreversible or allosteric antagonist change the affinity of the agonist to the receptor?

A

No, it will not be changed however Emax will be reduced in both cases.

71
Q

What kind of antagonists are irreversible and allosteric?

A

Non-competitive

72
Q

What does a non-competitive antagonist mean?

A

Adding more agonist will not increase the binding of the agents, same affinity for binding

73
Q

What do noncompetitive antagonists do?

A

They bind and inactivate a portion of receptors, which will reduce agonist efficacy (Emax)

74
Q

What is the effect of non-competitive antagonists?

A

Downward shift of Emax with no shift of potency

75
Q

What is a functional antagonist?

A

May act at a completely separate receptor, initiating effects that are functionally opposite than those of the agonist.

76
Q

What are competitive antagonists?

A

Compete with the agonist for the same binding site on the receptor.

77
Q

Why would a higher amount of agonist be needed if dealing with competitive antagonists?

A

The antagonist will try to displace agonist from their binding receptors

78
Q

What happens to the agonist’s affinity in the presence of a competitive antagonist?

A

Affinity for binding will be decreased

79
Q

What happens to competitive antagonists at high concentrations of agonist?

A

Competitive antagonists will be displaced from the receptor binding sites, Emax of agonist alone will be similar to Emax of agonist-antagonist.

80
Q

What are competitive antagonists used for in clinical scenarios?

A

Used to prevent the activity of drugs, and to reverse the effects of the drugs that have been consumed

81
Q

How does the presence of a competitive antagonist impact the affinity of the agonist?

A

It will affect it, increase the EC50, but Emax will be similar at high dose of antagonist.

82
Q

What are quantal dose-repose curved useful for?

A

Determining doses to which most of the population responds.

83
Q

What is the therapeutic index?

A

The ratio of the dose that produces toxicity in half the population to the dose that produces a clinically desired response in half the population.

84
Q

What is the therapeutic index used for?

A

Measure the drug’s safety

85
Q

Interpretation of therapeutic index:

A

A larger value indicates a wide margin between doses that are effective and doses that are toxic.

MEDI 202 - Genes To Community (23 decks)

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